CD4 T-cell

• CD4陽性T細胞

関

CD4-positive T-lymphocyte

WordNet

1. small room in which a monk or nun lives (同)cubicle
2. a device that delivers an electric current as the result of a chemical reaction (同)electric cell
3. a room where a prisoner is kept (同)jail cell, prison cell
4. (biology) the basic structural and functional unit of all organisms; they may exist as independent units of life (as in monads) or may form colonies or tissues as in higher plants and animals
5. any small compartment; "the cells of a honeycomb"
6. a small unit serving as part of or as the nucleus of a larger political movement (同)cadre
7. the 3rd letter of the Roman alphabet (同)c
8. (music) the keynote of the scale of C major
9. a general-purpose programing language closely associated with the UNIX operating system
10. the 20th letter of the Roman alphabet (同)t
11. a tough youth of 1950s and 1960s wearing Edwardian style clothes (同)Teddy boy

PrepTutorEJDIC

1. (刑務所の)『独房』;(修道院の)小さい独居室 / (ミツバチの)みつ房,巣穴 / 小さい部屋 / 『細胞』 / 電池 / 花粉室 / (共産党などの)細胞
2. carbonの化学記号
3. tritiumの化学記号
4. certificate of deposit / (また『C.D.』)Civil Defense民間防衛

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/11/14 08:05:46」(JST)

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T helper cells (T_h cells) are a sub-group of lymphocytes, a type of white blood cell, that play an important role in the immune system, particularly in the adaptive immune system. They help the activity of other immune cells by releasing T cell cytokines. They are essential in B cell antibody class switching, in the activation and growth of cytotoxic T cells, and in maximizing bactericidal activity of phagocytes such as macrophages.

Mature T_h cells express the surface protein CD4 and are referred to as CD4⁺ T cells. CD4⁺ T cells are generally treated as having a pre-defined role as helper T cells within the immune system. For example, when an antigen presenting cell expresses an antigen on MHC class II, a CD4⁺ cell will aid those cells through a combination of cell to cell interactions (e.g. CD40 and CD40L) and through cytokines. Nevertheless, there are rare exceptions; for example, sub-groups of regulatory T cells, natural killer T cells, and cytotoxic T cells express CD4 (although cytotoxic examples have been observed in extremely low numbers in specific disease states, they are usually considered non-existent). All of the latter CD4⁺ T cell groups are not considered T helper cells.

The importance of helper T cells can be seen from HIV, a virus that infects CD4⁺ cells. Towards the end of an HIV infection the number of functional CD4⁺ T cells falls, which leads to the symptomatic stage of infection known as the acquired immunodeficiency syndrome (AIDS). There are also some rare disorders that result in the absence or dysfunction of CD4⁺ T cells. These disorders produce similar symptoms, and many of these are fatal.

Activation of naïve helper T cells

Following T cell development, matured, naïve T cells leave the thymus and begin to spread throughout the body, including the lymph nodes. (Naïve T cells are those T cells that have never been exposed to the antigen that they are programmed to respond to). Like all T cells, they express the T cell receptor-CD3 complex. The T cell receptor (TCR) consists of both constant and variable regions. The variable region determines what antigen the T cell can respond to. CD4⁺ T cells have TCRs with an affinity for Class II MHC, and CD4 is involved in determining MHC affinity during maturation in the thymus. Class II MHC proteins are generally only found on the surface of specialised antigen-presenting cells (APCs). Specialised antigen presenting cells are primarily dendritic cells, macrophages and B cells, although B cells are the only cell group that expresses MHC Class II constitutively (at all times). Some APCs also bind native (or unprocessed) antigens to their surface, such as follicular dendritic cells, but unprocessed antigens do not interact with T cells and are not involved in their activation. The antigens that bind to MHC proteins are always short peptides, 8-10 amino acids long for MHC Class I, and up to 25 or so for MHC Class II.

Recognition (Signal 1)

During an immune response, professional antigen-presenting cells (APCs) endocytose foreign material (typically bacteria or viruses), which undergoes processing, then travel from the infection site to the lymph nodes. Once at the lymph nodes, the APC begin to present antigen peptides that are bound to Class II MHC, allowing CD4⁺ T cells that express the specific TCRs against the peptide/MHC complex to activate.

When a T_h cell encounters and recognises the antigen on an APC, the TCR-CD3 complex binds strongly to the peptide-MHC complex present on the surface of professional APCs. CD4, a co-receptor of the TCR complex, also binds to a different section of the MHC molecule. These interactions bring these proteins closer together, allowing the intracellular kinases present on the TCR, CD3 and CD4 proteins to activate each other via phosphorylation. With the assistance of a phosphatase present on the intracellular section of CD45 (common leukocyte antigen), these molecules activate major T_h cell intracellular pathways. These active pathways are known as Signal 1 of T cell activation, as it is the first and primary pro-activation signal in a T_h cell. Upon subsequent encounters with a given antigen, memory T cells are re-activated using the same TCR pathways.

The binding of the antigen-MHC to the TCR complex and CD4 may also help the APC and the T_h cell adhere during T_h cell activation, but the integrin protein LFA-1 on the T cell and ICAM on the APC are the primary molecules of adhesion in this cell interaction.

It is unknown what role the relatively bulky extracellular region of CD45 plays during cell interactions, but CD45 has various isoforms that change in size depending on the T_h cell's activation and maturation status. For example, CD45 shortens in length following T_h activation (CD45RA⁺ to CD45RO⁺), but whether this change in length influences activation is unknown. It has been proposed that the larger CD45RA+ may decrease the accessibility of the T cell receptor for the antigen-MHC molecule, thereby necessitating an increase in the affinity (and specificity) of the T cell for activation. Once the activation has occurred however, CD45 shortens, allowing easier interactions and activation as an effector T helper cell.^{[citation needed]}

Verification (Signal 2)

Having received the first TCR/CD3 signal, the naïve T cell must activate a second independent biochemical pathway, known as Signal 2. This verification step is a protective measure to ensure that a T cell is responding to a foreign antigen. If this second signal is not present during initial antigen exposure, the T cell presumes that it is auto-reactive. This results in the cell becoming anergic (anergy is generated from the unprotected biochemical changes of Signal 1). Anergic cells will not respond to any antigen in the future, even if both signals are present later on. These cells are generally believed to circulate throughout the body with no value until they undergo apoptosis.

The second signal involves an interaction between CD28 on the CD4⁺ T cell and the proteins CD80 (B7.1) or CD86 (B7.2) on the professional APCs. Both CD80 and CD86 activate the CD28 receptor. These proteins are also known as co-stimulatory molecules.

Although the verification stage is necessary for the activation of naïve helper T cells, the importance of this stage is best demonstrated during the similar activation mechanism of CD8⁺ cytotoxic T cells. As naïve CD8⁺ T cells have no true bias towards foreign sources, these T cells must rely on the activation of CD28 for confirmation that they recognise a foreign antigen (as CD80/CD86 is only expressed by active APC's). CD28 plays an important role in decreasing the risk of T cell auto-immunity against host antigens.

Once the naïve T cell has both pathways activated, the biochemical changes induced by Signal 1 are altered, allowing the cell to activate instead of anergise. The second signal is then obsolete; only the first signal is necessary for future activation. This is also true for memory T cells, which is one example of learned immunity. Faster responses occur upon reinfection because memory T cells have already undergone confirmation and can produce effector cells much sooner.

Proliferation

Once the two-signal activation is complete the T helper cell (T_h) then allows itself to proliferate. It achieves this by releasing a potent T cell growth factor called interleukin 2 (IL-2) which acts upon itself in an autocrine fashion. Activated T cells also produce the alpha sub-unit of the IL-2 receptor (CD25 or IL-2R), enabling a fully functional receptor that can bind with IL-2, which in turn activates the T cell's proliferation pathways.

The autocrine or paracrine secretion of IL-2 can bind that same T_h cell or neighboring T_h's via the IL-2R thus driving proliferation and clonal expansion. The T_h cells receiving both signals of activation will then become T_h0 cells (T helper 0) cell that secrete IL-2, IL-4 and interferon gamma (IFN-γ). The T_h0 cells will then differentiate into T_h1 or T_h2 cells depending on cytokine environment. IFN-γ drives T_h1 cell production while IL-10 and IL-4 inhibit T_h1 cell production. Conversely, IL-4 drives T_h2 cell production and IFN-γ inhibits T_h2 cells. It should be noted that these cytokines are pleiotropic and carry out many other functions of the immune response.

Maturation

After many cell generations, the T_h cell's progenitors differentiate into effector T_h cells, memory T_h cells, and regulatory T_h cells.

• Effector T_h cells secrete cytokines, proteins or peptides that stimulate or interact with other leukocytes, including T_h cells.

• Memory T_h cells retain the antigen affinity of the originally activated T cell, and are used to act as later effector cells during a second immune response (e.g. if there is re-infection of the host at a later stage).

• Regulatory T cells do not promote immune function, but act to decrease it instead. Despite their low numbers during an infection, these cells are believed to play an important role in the self-limitation of the immune system; they have been shown to prevent the development of various auto-immune diseases.

Determination of the effector T cell response

Helper T cells are capable of influencing a variety of immune cells, and the T cell response generated (including the extracellular signals such as cytokines) can be essential for a successful outcome from infection. In order to be effective, helper T cells must determine which cytokines will allow the immune system to be most useful or beneficial for the host. Understanding exactly how helper T cells respond to immune challenges is currently of major interest in immunology, because such knowledge may be very useful in the treatment of disease and in increasing the effectiveness of vaccination.

T_h1/T_h2 Model for helper T cells

Proliferating helper T cells that develop into effector T cells differentiate into two major subtypes of cells known as T_h1 and T_h2 cells (also known as Type 1 and Type 2 helper T cells, respectively).

T_h1 helper cells are the host immunity effectors against intracellular bacteria and protozoa. They are triggered by IL-12, IL-2 and their effector cytokine is IFN-γ. The main effector cells of T_h1 immunity are macrophages as well as CD8 T cells, IgG B cells, and IFN-γ CD4 T cells. The key T_h1 transcription factors are STAT4 and T-bet. IFN-γ secreted by CD4 T cells can activate macrophages to phagocytose and digest intracellular bacteria and protozoa. In addition, IFN-γ can activate iNOS to produce NOx free radicals to directly kill intracellular bacteria and protozoa. T_h1 overactivation against autoantigens will cause Type4 delayed-type hypersensitivity. Tuberculin reaction or Type 1 diabetes belong to this category of autoimmunity.

T_h2 helper cell are the host immunity effectors against multicellular helminths. They are triggered by IL-4 and their effector cytokines are IL-4, IL-5, and IL-13. The main effector cells are eosinophils, basophils, and mast cells as well as IgE B cells, and IL-4/IL-5 CD4 T cells. The key T_h2 transcription factors are STAT6 and GATAs. IL-5 from CD4 T cells will activate eosinophils to attack helminths. Besides, IL-4 and IgE will stimulate mast cells to release histamine, serotonin, and leukotriene to cause broncho-constriction, intestinal peristalsis, gastric fluid acidification to expel helminths. T_h2 overactivation against autoantigen will cause Type1 IgE-mediated allergy and hypersensitivity. Allergic rhinitis, atopic dermatitis, and asthma belong to this category of autoimmunity.

T_h1/T_h2 Model for helper T cells. An antigen is ingested and processed by an APC. It presents fragments from it to T cells. The upper, T_h0, is a T helper cell. The fragment is presented to it by MHC2. IFN-γ, interferon γ; TGF-β, transforming growth factor β; mø, macrophage; IL-2, interleukin 2; IL-4, interleukin 4

	Type 1/ Th1	Type 2/ Th2
Main partner cell type	Macrophage	B-cell
Cytokines produced	interferon-γ and TGF-beta. (Interleukin-2 was classically associated with Th1 cells, but this association may be misleading; IL-2 is produced by all helper T cells early in their activation.) interleukin-10 production has been shown to be induced in activated Th1 cell	interleukin-4, interleukin-5, interleukin-6, interleukin-10, interleukin-13
Immune stimulation promoted	Cellular immune system. Maximizes the killing efficacy of the macrophages and the proliferation of cytotoxic CD8+ T cells. Also promotes the production of opsonizing antibodies	Humoral immune system. Stimulates B-cells into proliferation, to induce B-cell antibody class switching, and to increase neutralizing antibody production.
Other functions	The Type 1 cytokine IFN-γ increases the production of interleukin-12 by dendritic cells and macrophages, and via positive feedback, IL-12 stimulates the production of IFN-γ in helper T cells, thereby promoting the Th1 profile. IFN-gamma also inhibits the production of cytokines such as interleukin-4, an important cytokine associated with the Type 2 response, and thus it also acts to preserve its own response.	The Type 2 response promotes its own profile using two different cytokines. Interleukin-4 acts on helper T cells to promote the production of Th2 cytokines (including itself; it is auto-regulatory), while interleukin-10 (IL-10) inhibits a variety of cytokines including interleukin-2 and IFN-γ in helper T cells and IL-12 in dendritic cells and macrophages. The combined action of these two cytokines suggests that once the T cell has decided to produce these cytokines, that decision is preserved (and also encourages other T cells to do the same).

While we know about the types of cytokine patterns helper T cells tend to produce, we understand less about how the patterns themselves are decided. Various evidence suggests that the type of APC presenting the antigen to the T cell has a major influence on its profile. Other evidence suggests that the concentration of antigen presented to the T cell during primary activation influences its choice. The presence of some cytokines (such as the ones mentioned above) will also influence the response that will eventually be generated, but our understanding is nowhere near complete.

TH17 helper cells

TH17 helper cells mediate host immunity against extracellular bacteria and fungi. It is triggered by IL-6 and TGF beta. Its main effector cytokines are IL-6, IL1, and TNF alpha. The main TH17 effector cells are neutrophils as well as IgM/IgA B cells, and IL-17 CD4 T cells. The key Th17 transcription factors are STAT3 and RORg. TNF alpha can activate neutrophils to kill extracellular bacteria and fungi. Besides, Il-6 can upregulate the complement system to directly kill extracellular bacteria and fungi. TH17 overactivation against autoantigen will cause type 3 immune complex and complement-mediated hypersensitivity. Rheumatoid arthritis or Arthus reaction belong to this category.

THαβ helper cells

THαβ helper cells provide the host immunity against viruses. Their differentiation is triggered by IFN alpha/beta or IL-10. Their key effector cytokine is IL-10. Their main effector cells are NK cells as well as CD8 T cells, IgG B cells, and IL-10 CD4 T cells. The key THαβ transcription factors are STAT1 and STAT3 as well as IRFs. IL-10 from CD4 T cells activate NK cells' ADCC to apoptose virus-infected cells and to induce host as well as viral DNA fragmentation. IFN alpha/beta can suppress transcription to avoid virus replication and transmission. Overactivation of THαβ against autoantigen will cause type 2 antibody-dependent cytotoxic hypersensitivity. Myasthenia gravis or Graves' disease belong to this category.

Limitations to the T_h1/T_h2 model

The interactions between cytokines from the T_h1/T_h2 model can be more complicated in some animals. For example, the T_h2 cytokine IL-10 inhibits cytokine production of both T_h subsets in humans. Human IL-10 (hIL-10) suppresses the proliferation and cytokine production of all T cells and the activity of macrophages, but continues to stimulate plasma cells, ensuring that antibody production still occurs. As such, hIL-10 is not believed to truly promote the T_h2 response in humans, but acts to prevent over-stimulation of helper T cells while still maximising the production of antibodies.

There are also other types of T cells that can influence the expression and activation of helper T cells, such as natural regulatory T cells, along with less common cytokine profiles such as the T_h3 subset of helper T cells. Terms such as "regulatory" and "suppression" have become ambiguous after the discovery that helper CD4⁺ T cells are also capable of regulating (and suppressing) their own responses outside of dedicated regulatory T cells.

One major difference between regulatory T cells and effector T cells is that regulatory T cells typically serve to modulate and deactivate the immune response, while effector T cell groups usually begin with immune-promoting cytokines and then switch to inhibitory cytokines later in their life cycle. The latter is a feature of T_h3 cells, which transform into a regulatory subset after its initial activation and cytokine production.

Both regulatory T cells and T_h3 cells produce the cytokine transforming growth factor-beta (TGF-β) and IL-10. Both cytokines are inhibitory to helper T cells; TGF-β suppresses the activity of most of the immune system. There is evidence to suggest that TGF-β may not suppress activated Th2 cells as effectively as it might suppress naive cells, but it is not typically considered a Th2 cytokine.

The characterisation of another novel T helper subtype, T helper 17 cells (T_h17) has cast further doubt on the basic T_h1/T_h2 model. These IL-17 producing cells were initially described as a pathogenic population implicated in autoimmunity but are now thought to have their own distinct effector and regulatory functions. Of note, recent evidence suggest that functional plasticity is an intrinsic capacity of T helper cells. Indeed, a study in mice demonstrated that T_h17 cells transform into T_h1 cells in vivo. A subsequent study furthermore showed that extensive T helper cell plasticity is also prominent in man.

Many of the cytokines in this article are also expressed by other immune cells (see individual cytokines for details), and it is becoming clear that while the original T_h1/T_h2 model is enlightening and gives insight into the functions of helper T cells, it is far too simple to define its entire role or actions. Some immunologists question the model completely, as some in vivo studies suggest that individual helper T cells usually do not match the specific cytokine profiles of the T_h model, and many cells express cytokines from both profiles. That said, the T_h model has still played an important part in developing our understanding of the roles and behaviour of helper T cells and the cytokines they produce during an immune response.

Recent scientific studies by Stockinger et al. revealed that another T helper subset may exist. Th9 cells are claimed to be an IL9 (interleukin 9)–producing T cell subset focused on defending helminth infections.

Role of helper T cells in disease

Considering the diverse and important role helper T cells play in the immune system, it is not surprising that these cells often influence the immune response against disease. They also appear to make occasional mistakes, or generate responses that would be politely considered non-beneficial. In the worst case scenario, the helper T cell response could lead to a disaster and the fatality of the host. Fortunately this is a very rare occurrence.

Helper T cells and hypersensitivity

The immune system must achieve a balance of sensitivity in order to respond to foreign antigens without responding to the antigens of the host itself. When the immune system responds to very low levels of antigen that it usually shouldn't respond to, a hypersensitivity response occurs. Hypersensitivity is believed to be the cause of allergy and some auto-immune disease.

Hypersensitivity reactions can be divided into four types:

• Type 1 hypersensitivity includes common immune disorders such as asthma, allergic rhinitis (hay fever), eczema, urticaria (hives) and anaphylaxis. These reactions all involve IgE antibodies, which require a T_h2 response during helper T cell development. Preventive treatments, such as corticosteroids and montelukast, focus on suppressing mast cells or other allergic cells; T cells do not play a primary role during the actual inflammatory response. It's important to note that the numeral allocation of hypersensitivity "types" does not correlate (and is completely unrelated) to the "response" in the T_h model.

• Type 2 and Type 3 hypersensitivity both involve complications from auto-immune or low affinity antibodies. In both of these reactions, T cells may play an accomplice role in generating these auto-specific antibodies, although some of these reactions under Type 2 hypersensitivity would be considered normal in a healthy immune system (for example, Rhesus factor reactions during child-birth is a normal immune response against child antigens). The understanding of the role of helper T cells in these responses is limited but it is generally thought that T_h2 cytokines would promote such disorders. For example, studies have suggested that lupus (SLE) and other auto-immune diseases of similar nature can be linked to the production of T_h2 cytokines.

• Type 4 hypersensitivity, also known as delayed type hypersensitivity, are caused via the over-stimulation of immune cells, commonly lymphocytes and macrophages, resulting in chronic inflammation and cytokine release. Antibodies do not play a direct role in this allergy type. T cells play an important role in this hypersensitivity, as they activate against the stimulus itself and promote the activation of other cells; particularly macrophages via T_h1 cytokines.

Other cellular hypersensitivities include cytotoxic T cell mediated auto-immune disease, and a similar phenomenon; transplant rejection. Helper T cells are required to fuel the development of these diseases. In order to create sufficient auto-reactive killer T cells, interleukin-2 must be produced, and this is supplied by CD4⁺ T cells. CD4⁺ T cells can also stimulate cells such as natural killer cells and macrophages via cytokines such as interferon-gamma, encouraging these cytotoxic cells to kill host cells in certain circumstances.

The mechanism that killer T cells use during auto-immunity is almost identical to their response against viruses, and some viruses have been accused of causing auto-immune diseases such as Type 1 Diabetes mellitus. Cellular auto-immune disease occurs because the host antigen recognition systems fail, and the immune system believes, by mistake, that a host antigen is foreign. As a result, the CD8⁺ T cells treat the host cell presenting that antigen as infected, and go on to destroy all host cells (or in the case of transplant rejection, transplant organ) that express that antigen.

Some of this section is a simplification. Many auto-immune diseases are more complex. A well-known example is rheumatoid arthritis, where both antibodies and immune cells are known to play a role in the pathology. Generally the immunology of most auto-immune diseases is not well understood.

HIV infection

Perhaps the best example of the importance of CD4⁺ T cells is demonstrated with human immunodeficiency virus (HIV) infection. HIV targets cells that express CD4, and can infect macrophages, dendritic cells (both groups express CD4 at low levels) and CD4⁺ T cells.

It has been proposed that during the non-symptomatic phase of HIV infection, the virus has a relatively low affinity towards T cells (and has a higher affinity for macrophages), resulting in a slow kill rate of CD4⁺ T cells by the immune system^{[citation needed]}. This is initially compensated for via the production of new helper T cells from the thymus (originally from the bone marrow). Once the virus becomes lymphotropic (or T-tropic) however, it begins to infect CD4⁺ T cells far more efficiently (likely due to a change in the co-receptors it binds to during infection), and the immune system is overwhelmed.

At this point, functional CD4⁺ T cell levels begin to decrease, eventually to a point where the CD4⁺ T cell population is too small to recognize the full range of antigens that could potentially be detected. The lack of full antigen cover results in the core symptoms of acquired immune deficiency syndrome (AIDS). CD4 T cell depletion during AIDS allows various pathogens to escape T cell recognition, thus allowing opportunistic infections that would normally elicit a helper T cell response to bypass the immune system. While these complete bypass situations only occur when the helper T cell response is absolutely necessary for infection clearance, most infections increase in severity and/or duration because the immune system's helper T cells provide a weaker contribution to a less efficient immune response.

Two components of the immune system are particularly affected in AIDS, due to its CD4⁺ T cell dependency:

1. CD8⁺ T cells are not stimulated as effectively during the AIDS stage of HIV infection, making AIDS patients very susceptible to most viruses, including HIV itself. This decline in killing of CD4⁺ T cells results in the virus being produced for a longer period (the infected CD4⁺ T cells are not killed as quickly), increasing the proliferation of the virus, and accelerating the development of the disease.
2. Antibody class switching declines significantly once helper T cell function fails. The immune system loses its ability to improve the affinity of their antibodies, and are unable to generate B cells that can produce antibody groups such as IgG and IgA. These effects are primarily due to the loss of any helper T cell that can interact with the B lymphocyte correctly. Another symptom of AIDS is the reduction in antibody levels due to a decrease in T_h2 cytokines (and less interactions by helper T cells). All of these complications result in an increased susceptibility to aggressive bacterial infections, especially in areas of the body not accessible by IgM antibodies.

If the patient does not respond to (or does not receive) HIV treatment they will succumb usually to either cancers or infections; the immune system finally reaches a point where it is no longer coordinated or stimulated enough to deal with the disease.

Inhibition of CD4 T-cell expansion during HIV infection is also due to microbial translocation in an IL-10-dependent way. Indeed, triggering PD-1, expressed on monocytes and up-regulated upon monocytes activation, by its ligand PD-L1 induces IL-10 production which inhibits CD4 T-cell function.

See also

• Cd4+ T cells and antitumor Immunity

References

• In SLE patients, T helper type 1 polarisation is more abundant rather than type 2, where the main cytokine profile are Inf gama from T cells and its consequence interferon alpha high range production by DC .

External links

• T-cell Group - Cardiff University

UpToDate Contents

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• 1. ヘルパーT細胞サブセット：疾患における分化および役割 t helper subsets differentiation and role in disease
• 2. 適応細胞性免疫応答 the adaptive cellular immune response
• 3. 移植免疫 transplantation immunobiology
• 4. BおよびTリンパ球の正常な発生 normal b and t lymphocyte development
• 5. 癌免疫療法の原則 principles of cancer immunotherapy

English Journal

• Electrochemical magneto-actuated biosensor for CD4 count in AIDS diagnosis and monitoring.

• Carinelli S1, Xufré Ballesteros C2, Martí M2, Alegret S1, Pividori MI3.
• Biosensors & bioelectronics.Biosens Bioelectron.2015 Dec 15;74:974-80. doi: 10.1016/j.bios.2015.07.053. Epub 2015 Jul 26.
• The counting of CD4(+) T lymphocytes is a clinical parameter used for AIDS diagnosis and follow-up. As this disease is particularly prevalent in developing countries, simple and affordable CD4 cell counting methods are urgently needed in resource-limited settings. This paper describes an electrochem
• PMID 26264263

• Induction of CD4(+) and CD8(+) anti-tumor effector T cell responses by bacteria mediated tumor therapy.

• Stern C1, Kasnitz N1, Kocijancic D1, Trittel S2, Riese P2, Guzman CA2, Leschner S1, Weiss S1.
• International journal of cancer. Journal international du cancer.Int J Cancer.2015 Oct 15;137(8):2019-28. doi: 10.1002/ijc.29567. Epub 2015 May 9.
• Facultative anaerobic bacteria like E. coli can colonize solid tumors often resulting in tumor growth retardation or even clearance. Little mechanistic knowledge is available for this phenomenon which is however crucial for optimization and further implementation in the clinic. Here, we show that in
• PMID 25868911

• Elevated IFN-alpha/beta levels in a streptozotocin-induced type I diabetic mouse model promote oxidative stress and mediate depletion of spleen-homing CD8+ T cells by apoptosis through impaired CCL21/CCR7 axis and IL-7/CD127 signaling.

• Mahmoud MH1, Badr G2, Badr BM3, Kassem AU4, Mohamed MS4.
• Cellular signalling.Cell Signal.2015 Oct;27(10):2110-9. doi: 10.1016/j.cellsig.2015.07.005. Epub 2015 Jul 18.
• Type 1 diabetes mellitus (T1D) is associated with increased type 1 interferon (IFN) levels and subsequent severe defects in lymphocyte function, which increase susceptibility to infections. The blockade of type 1 IFN receptor 1 (IFNAR1) in non-obese diabetic mice has been shown to delay T1D onset an
• PMID 26192098

Japanese Journal

• TGF-β3発現CD4⁺CD25⁻LAG3⁺制御性T細胞による全身性自己免疫応答制御 (特集 全身性免疫疾患の機序の解明)

• 臨床免疫・アレルギー科 = Clinical immunology & allergology 65(2), 126-131, 2016-02
• NAID 40020741944

• HTLV-1 bZIP Factor Impairs Anti-viral Immunity by Inducing Co-inhibitory Molecule, T Cell Immunoglobulin and ITIM Domain (TIGIT)

• PLOS Pathogens 12(1), 2016-01-06
• NAID 120005763385

• Progressive Multifocal Leukoencephalopathy with Balanced CD4/CD8 T-Cell Infiltration and Good Response to Mefloquine Treatment

• Internal Medicine 55(12), 1631-1635, 2016
• NAID 130005157669

Related Links

• T細胞 （T cell） - 東邦大学理学部

Tリンパ球とも言う。T細胞は、細胞表面のCD4およびCD8というT細胞特異的に発現するタンパク質の発現パターンを指標として分化が進行していき、骨髄内の造血幹細胞から派生した先駆（プロ）T細胞（CD4-CD8-T細胞）は、胸腺へと移動 ...

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Related Pictures

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★リンクテーブル★

リンク元	「CD4陽性T細胞」「CD4-positive T-lymphocyte」
関連記事	「C」「CD」「T」「CD4」「cell」

「CD4陽性T細胞」

　　[★]

英

CD4 T-cell、CD4-positive T-lymphocyte

関

CD4陽性Tリンパ球、T4リンパ球、CD4陽性リンパ球、T4細胞

「CD4-positive T-lymphocyte」

　　[★]

CD4陽性T細胞、CD4陽性Tリンパ球

関

CD4 T-cell、CD4-positive lymphocyte、T4 cell、T4 lymphocyte

「C」

　　[★]

• 炭素 carbon
• シトシン cytosine
• システイン cysteine
• シチジン
• セルシウス度 摂氏 degrees Celsius degree C
• 産婦人科領域で「子宮外頚 子宮外頚部 exocervix」を表現するための略語

　 　 　 　

「CD」

　　[★]

• 表面抗原分類 cluster of differentiation
• 膠原病 collagen disease
• 集合管 collecting duct
• クローン病 Crohn's disease

　

「T」

　　[★]

• T波 T wave
• チミン thymine
• ツイスト数
• スレオニントレオニン threonine

　 　

「CD4」

　　[★]

同

T4, Leucine-SA, Leucine-3B

関

表面抗原分類

「cell」

　　[★] 細胞