Toll-like receptor 4

同

TLR-4

同

TLR-4

WordNet

1. want to have; "Id like a beer now!"
2. a kind of person; "Well not see his like again"; "I cant tolerate people of his ilk" (同)ilk
3. a similar kind; "dogs, foxes, and the like", "we dont want the likes of you around here" (同)the like, the likes of
4. equal in amount or value; "like amounts"; "equivalent amounts"; "the same amount"; "gave one six blows and the other a like number"; "the same number" (同)same
5. resembling or similar; having the same or some of the same characteristics; often used in combination; "suits of like design"; "a limited circle of like minds"; "members of the cat family have like dispositions"; "as like as two peas in a pod"; "doglike devotion"; "a dreamlike quality" (同)similar
6. be fond of; "I like my nephews"
7. feel about or towards; consider, evaluate, or regard; "How did you like the Presidents speech last night?"
8. find enjoyable or agreeable; "I like jogging"; "She likes to read Russian novels"
9. ring slowly; "For whom the bell tolls"
10. a fee levied for the use of roads or bridges (used for maintenance)
11. charge a fee for using; "Toll the bridges into New York City"
12. a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
13. a feeling of pleasure and enjoyment; "Ive always had a liking for reading"; "she developed a liking for gin"
14. found pleasant or attractive; often used as a combining form; "a well-liked teacher"

PrepTutorEJDIC

1. …‘を'『好む』,‘が'好きである / 《しばしば否定文で,またwould,《英》shouldと共に用いて》…‘を'望む,…したい / 『好む』;望む / 《複数形で》好み,好きな事
2. (外観・性質などが)…『に似た』,のような / (やり方,程度などが)…『と同じように』 / …『らしい』,にふさわいし / 《おもに話》たとえば…のような / 《名詞の前にのみ用いて》(性質・外観などが)同じの,(数量が)等しい / 《補語にのみ用いて》似ている,そっくりで / たぶん,おそらく(probably) / (…に)似た人(物),(…と)同等の人(物),匹敵する人(物)《+『of』+『名』》 / …のように / あたかも…のように
3. 〈鐘が〉(にっくり規則的に繰り返して)鳴る / (ゆっくり規則的に繰り返して)〈鐘〉‘を'鳴らす / 〈鐘が〉…‘を'知らせる / 鐘を鳴らすこと / 鐘の音
4. (橋・道路などの)『使用[通行]料金』,使用税 / (長距離電話などの)『料金』,サービス料 / 《通例単数形で》(災難などの)被害の程度,犠牲(死傷)負数
5. =sense organ / 受信装置
6. (…の)『好み』,趣味《+『for』(『to』)+『名』》

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/09/24 11:19:51」(JST)

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TLR4
Available structures PDB Ortholog search: PDBe RCSB List of PDB id codes 4G8A, 2Z62, 2Z63, 2Z65, 2Z66, 3FXI, 3UL7, 3UL8, 3UL9, 3ULA
Identifiers
Aliases	TLR4, ARMD10, CD284, TLR-4, TOLL, toll like receptor 4
External IDs	OMIM: 603030 MGI: 96824 HomoloGene: 41317 GeneCards: TLR4
Gene location (Human) Chr. Chromosome 9 (human) Band 9q33.1 Start 117,704,332 bp End 117,716,871 bp
Gene location (Mouse) Chr. Chromosome 4 (mouse) Band n/a Start 66,827,584 bp End 66,930,284 bp
RNA expression pattern More reference expression data
Gene ontology Molecular function • lipopolysaccharide receptor activity • lipopolysaccharide binding • protein binding • transmembrane signaling receptor activity • receptor activity Cellular component • cytoplasm • membrane • perinuclear region of cytoplasm • cell surface • integral component of membrane • plasma • endosome membrane • intrinsic component of plasma membrane • integral component of plasma membrane • lipopolysaccharide receptor complex • external side of plasma membrane Biological process • positive regulation of MHC class II biosynthetic process • positive regulation of JNK cascade • TRIF-dependent toll-like receptor signaling pathway • positive regulation of interleukin-12 biosynthetic process • cellular response to mechanical stimulus • positive regulation of interleukin-8 production • positive regulation of ERK1 and ERK2 cascade • T-helper 1 type immune response • interferon-gamma production • positive regulation of platelet activation • positive regulation of interleukin-1 production • positive regulation of stress-activated MAPK cascade • positive regulation of NLRP3 inflammasome complex assembly • positive regulation of interleukin-12 production • positive regulation of interferon-alpha production • regulation of cytokine secretion • positive regulation of interferon-beta biosynthetic process • I-kappaB phosphorylation • positive regulation of nitric-oxide synthase biosynthetic process • interleukin-1 beta secretion • positive regulation of B cell proliferation • defense response to bacterium • positive regulation of interleukin-6 production • activation of innate immune response • positive regulation of tumor necrosis factor production • positive regulation of interleukin-8 biosynthetic process • negative regulation of tumor necrosis factor production • innate immune response • negative regulation of interleukin-17 production • I-kappaB kinase/NF-kappaB signaling • positive regulation of interferon-beta production • positive regulation of inflammatory response • toll-like receptor 4 signaling pathway • positive regulation of macrophage cytokine production • positive regulation of tumor necrosis factor biosynthetic process • positive regulation of interleukin-10 production • immune system process • astrocyte development • intestinal epithelial structure maintenance • positive regulation of nucleotide-binding oligomerization domain containing 1 signaling pathway • response to lipopolysaccharide • activation of MAPK activity • cellular response to lipoteichoic acid • positive regulation of NF-kappaB transcription factor activity • immune response • negative regulation of interleukin-23 production • regulation of inflammatory response • positive regulation of chemokine production • lipopolysaccharide-mediated signaling pathway • detection of fungus • positive regulation of nucleotide-binding oligomerization domain containing 2 signaling pathway • negative regulation of interferon-gamma production • response to bacterium • negative regulation of osteoclast differentiation • B cell proliferation involved in immune response • positive regulation of nitric oxide biosynthetic process • negative regulation of interleukin-6 production • positive regulation of interferon-gamma production • nitric oxide production involved in inflammatory response • MyD88-dependent toll-like receptor signaling pathway • regulation of dendritic cell cytokine production • positive regulation of gene expression • negative regulation of ERK1 and ERK2 cascade • positive regulation of I-kappaB kinase/NF-kappaB signaling • macrophage activation • positive regulation of NF-kappaB import into nucleus • detection of lipopolysaccharide • cellular response to lipopolysaccharide • positive regulation of lymphocyte proliferation • positive regulation of transcription from RNA polymerase II promoter • MyD88-independent toll-like receptor signaling pathway • signal transduction • inflammatory response • defense response to Gram-negative bacterium • toll-like receptor signaling pathway • necroptotic process • apoptotic signaling pathway • negative regulation of MyD88-independent toll-like receptor signaling pathway Sources:Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	7099	21898
Ensembl	ENSG00000136869	ENSMUSG00000039005
UniProt	O00206	Q9QUK6
RefSeq (mRNA)	NM_138557 NM_003266 NM_138554 NM_138556	NM_021297
RefSeq (protein)	NP_003257 NP_612564 NP_612567	NP_067272
Location (UCSC)	Chr 9: 117.7 – 117.72 Mb	Chr 9: 66.83 – 66.93 Mb
PubMed search
Wikidata
View/Edit Human View/Edit Mouse

Toll-like receptor 4 is a protein that in humans is encoded by the TLR4 gene. TLR4 is a transmembrane protein, member of the toll-like receptor family, which belongs to the pattern recognition receptor (PRR) family. Its activation leads to an intracellular signaling pathway NF-κB and inflammatory cytokine production which is responsible for activating the innate immune system. It is most well known for recognizing lipopolysaccharide (LPS), a component present in many Gram-negative bacteria (e.g. Neisseria spp.) and select Gram-positive bacteria. Its ligands also include several viral proteins, polysaccharide, and a variety of endogenous proteins such as low-density lipoprotein, beta-defensins, and heat shock protein.

TLR 4 has also been designated as CD284 (cluster of differentiation 284). The molecular weight of TLR 4 is approximately 95 kDa.

Function

The protein encoded by this gene is a member of the toll-like receptor (TLR) family, which plays a fundamental role in pathogen recognition and activation of innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. They recognize pathogen-associated molecular patterns (PAMPs) that are expressed on infectious agents, and mediate the production of cytokines necessary for the development of effective immunity.

The various TLRs exhibit different patterns of expression. This receptor is most abundantly expressed in placenta, and in myelomonocytic subpopulation of the leukocytes.

It cooperates with LY96 (also referred as MD-2) and CD14 to mediate in signal transduction events induced by lipopolysaccharide (LPS) found in most gram-negative bacteria. Mutations in this gene have been associated with differences in LPS responsiveness.

TLR4 signaling responds to signals by forming a complex using an extracellular leucine-rich repeat domain (LRR) and an intracellular toll/interleukin-1 receptor (TIR) domain. LPS stimulation induces a series of interactions with several accessory proteins which form the TLR4 complex on the cell surface. LPS recognition is initiated by an LPS binding to an LBP protein. This LPS-LBP complex transfers the LPS to CD14. CD14 is a glycosylphosphatidylinositol-anchored membrane protein that binds the LPS-LBP complex and facilitates the transfer of LPS to MD-2 protein, which is associated with the extracellular domain of TLR4. LPS binding promotes the dimerization of TLR4/MD-2. The conformational changes of the TLR4 induce the recruitment of intracellular adaptor proteins containing the TIR domain which is necessary to activate the downstream signaling pathway.

Several transcript variants of this gene have been found, but the protein-coding potential of most of them is uncertain.

Most of the reported effects of TLR4 signaling in tumors are pro-carcinogenic mainly due to contributions of proinflammatory cytokine signaling (whose expression is driven by TLR-mediated signals) to tumor-promoting microenvironment.

Signaling

Upon LPS recognition, conformational changes in the TLR4 receptors result in recruitment of intracellular TIR-domains containing adaptor molecules. These adaptors are associated with the TLR4 cluster via homophilic interactions between the TIR domains. There are four adaptor proteins involved in two major intracellular signaling pathways.

Signaling pathway of toll-like receptor 4. Dashed grey lines represent unknown associations

MyD88 – Dependent Pathway

The MyD88-dependent pathway is regulated by two adaptor-associated proteins: Myeloid Differentiation Primary Response Gene 88 (MyD88) and TIR Domain-Containing Adaptor Protein (TIRAP). TIRAP-MyD88 regulates early NF-κβ activation and production of proinflammatory cytokines, such as IL-12. MyD88 signaling involves the activation of IL-1 Receptor-Associated Kinases (IRAKs) and the adaptor molecules TNF Receptor-Associated Factor 6 (TRAF6). TRAF6 induces the activation of TAK1 (Transforming growth factor-β-Activated Kinase 1) that leads to the activation of MAPK cascades (Mitogen-Activated Protein Kinase) and IKK (IκB Kinase). IKKs' signaling pathway leads to the induction of the transcription factor NF-κβ, while activation of MAPK cascades lead to the activation of another transcription factor AP-1. Both of them have a role in the expression of proinflammatory cytokines.

MyD88 – Independent Pathway

This TRIF-dependent pathway involves the recruitment of the adaptor proteins TIR-domain-containing adaptor inducing interferon-β (TRIF) and TRIF-related Adaptor Molecule (TRAM). TRAM-TRIF signals activate the transcription factor Interferon Regulatory Factor-3 (IRF3) via TRAF3. IRF3 activation induces the production of type 1 interferons.

SARM: Negative Regulator of the TRIF-mediated Pathway

A fifth TIR-domain-containing adaptor protein called Sterile α and HEAT (Armadillo motif) (SARM) is a TLR4 signaling pathway inhibitor. SARM activation by LPS-binding inhibits -TRIF-mediated pathways but does not inhibit MyD88-mediated pathways. This mechanism prevents an excessive activation in response to LPS which may lead to inflammation-induced damage such as sepsis.

Evolutionary history

TLR4 originated when TLR2 and TLR4 diverged about 500 million years ago near the beginning of vertebrate evolution. Sequence alignments of human and great ape TLR4 exons have demonstrated that not much evolution has occurred in human TLR4 since our divergence from our last common ancestor with chimpanzees; human and chimp TLR4 exons only differ by three substitutions while humans and baboons are 93.5% similar in the extracellular domain. Notably, humans possess a greater number of early stop codons in TLR4 than great apes; in a study of 158 humans worldwide, 0.6% had a nonsense mutation. This suggests that there are weaker evolutionary pressures on the human TLR4 than on our primate relatives. The distribution of human TLR4 polymorphisms matches the out-of-Africa migration, and it is likely that the polymorphisms were generated in Africa before migration to other continents.

Interactions

TLR 4 has been shown to interact with:

• Lymphocyte antigen 96,
• Myd88, and
• TOLLIP.

Intracellular trafficking of TLR4 is dependent on the GTPase Rab-11a, and knock down of Rab-11a results in hampered TLR4 recruitment to E. coli-containing phagosomes and subsequent reduced signal transduction through the MyD88-independent pathway.

Clinical significance

Various single nucleotide polymorphisms (SNPs) of the TLR4 in humans have been identified and for some of them an association with increased susceptibility to Gram-negative bacterial infections or faster progression and a more severe course of sepsis in critically ill patients was reported.

In cancer progression

TLR4 expression can be detected on many tumor cells and cell lines. TLR4 is capable of activating MAPK and NF-κB pathways, implicating possible direct role of cell-autonomous TLR4 signaling in regulation of carcinogenesis, in particular, through increased proliferation of tumor cells, apoptosis inhibition and metastasis. TLR4 signaling may also contribute to resistance to paclitaxel chemotherapy in ovary cancer and siRNA therapy in prostate cancer. 63% of breast cancer patients were reported to express TLR4 on tumor cells and the level of expression inversely correlated with the survival. Additionally, low MyD88 expression correlated with decreased metastasis to the lung and decreased CCL2 and CCL5 expression. TLR4 expression levels were the highest among TLRs in human breast cancer cell line MDA-MB-231 and TLR4 knockdown resulted in decreased proliferation and decreased IL-6 and IL-8 levels. On the other hand, TLR4 signaling in immune and inflammatory cells of tumor microenvironment may lead to production of proinflammatory cytokines (TNF, IL-1β, IL-6, IL-18, etc.), immunosuppressive cytokines (IL-10, TGF-β, etc.) and angiogenic mediators (VEGF, EGF, TGF-β, etc.). These activities may result in further polarization of tumor-associated macrophages, conversion of fibroblasts into tumor-promoting cancer-associated fibroblasts, conversion of dendritic cells into tumor-associated DCs and activation of pro-tumorigenic functions of immature myeloid cells - Myeloid-derived Suppressor Cells (MDSC). TLR signaling has been linked to accumulation and function of MDSC at the site of tumor and it also allows mesenchymal stromal cells to counter NK cell-mediated anti-tumor immunity. In HepG2 hepatoblastoma cells LPS increased TLR4 levels, cell proliferation and resistance to chemotherapy, and these phenomena could be reversed by TLR4 gene knockdown. Similarly, LPS stimulation of human liver cancer cell line H7402 resulted in TLR4 upregulation, NF-κB activation, TNF, IL-6 and IL-8 production and increased proliferation that could be reversed by signal transducer and STAT3 inhibition.Besides the well known successful usage of Bacillus Calmette–Guérin (BCG) in the therapy of bladder cancer there are reports on the treatment of oral squamous cell carcinoma, gastric cancer and cervical cancer with lyophilized streptococcal preparation OK-432 and utilization of TLR4/TLR2 ligands – derivatives of muramyl dipeptide.

In pregnancy

Activation of TLR4 in intrauterine infections leads to deregulation of prostaglandin synthesis, leading to uterine smooth muscle contraction.

Asp299Gly polymorphism

Classically, TLR4 is said to be the receptor for LPS, however TLR 4 has also been shown to be activated by other kinds of lipids. Plasmodium falciparum, a parasite known to cause the most common and serious form of malaria that is seen primarily in Africa, produces glycosylphosphatidylinositol, which can activate TLR4. Two SNPs in TLR4 are co-expressed with high penetrance in African populations (i.e. TLR-4-Asp299Gly and TLR-4-Thr399Ile). These Polymorphisms are associated with an increase in TLR4-Mediated IL-10 production—an immunomodulator—and a decrease in proinflammatory cytokines. The TLR-4-Asp299Gly point mutation is strongly correlated with an increased infection rate with Plasmodium falciparum. It appears that the mutation prevents TLR4 from acting as vigorously against, at least some plasmodial infections. The malaria infection rate and associated morbidity are higher in TLR-4-Asp299Gly group, but mortality appears to be decreased. This may indicate that at least part of the pathogenesis of malaria takes advantage of cytokine production. By reducing the cytokine production via the TLR4 mutation, the infection rate may increase, but the number of deaths due to the infection seem to decrease.

In addition, TLR4-D299G has been associated with aggressive colorectal cancer in humans. It has been shown that human colon adenocarcinomas from patients with TLR4-D299G were more frequently of an advanced stage with metastasis than those with wild-type TLR4. The same study demonstrated functionally that intestinal epithelial cells (Caco-2) expressing TLR4-D299G underwent epithelial-mesenchymal transition and morphologic changes associated with tumor progression, whereas intestinal epithelial cells expressing wild-type TLR4 did not.

Animal studies

A link between the TLR 4 receptor and binge drinking has been suggested. When genes responsible for the expression of TLR 4 and GABA receptors are manipulated in rodents that had been bred and trained to drink excessively, the animals showed a "profound reduction" in drinking behaviours. Additionally, it has been shown that ethanol, even in the absence of LPS, can activate TLR4 signaling pathways.

High levels of TLR4 molecules and M2 tumor-associated macrophages are associated with increased susceptibility to cancer growth in mice deprived of sleep. Mice genetically modified so that they could not produce TLR4 molecules showed normal cancer growth.

Drugs targeting TLR4

Toll-like receptor 4 has been shown to be important for the long-term side-effects of opioid analgesic drugs. Various μ-opioid receptor ligands have been tested and found to also possess action as agonists or antagonists of TLR4, with opioid agonists such as morphine being TLR4 agonists, while opioid antagonists such as naloxone were found to be TLR4 antagonists. Activation of TLR4 leads to downstream release of inflammatory modulators including TNF-α and Interleukin-1, and constant low-level release of these modulators is thought to reduce the efficacy of opioid drug treatment with time, and be involved in both the development of tolerance to opioid analgesic drugs, and in the emergence of side-effects such as hyperalgesia and allodynia that can become a problem following extended use of opioid drugs. Drugs that block the action of TNF-α or IL-1β have been shown to increase the analgesic effects of opioids and reduce the development of tolerance and other side-effects, and this has also been demonstrated with drugs that block TLR4 itself. Interestingly the response of TLR4 to opioid drugs has been found to be enantiomer-independent, so the "unnatural" enantiomers of opioid drugs such as morphine and naloxone, which lack affinity for opioid receptors, still produce the same activity at TLR4 as their "normal" enantiomers. This means that the unnatural enantiomers of opioid antagonists, such as (+)-naloxone, can be used to block the TLR4 activity of opioid analgesic drugs, while leaving the μ-opioid receptor mediated analgesic activity unaffected.) This may also be the mechanism behind the beneficial effect of ultra-low dose naltrexone on opioid analgesia.

Morphine causes inflammation by binding to the protein lymphocyte antigen 96, which, in turn, causes the protein to bind to Toll-like receptor 4 (TLR4). The morphine-induced TLR4 activation attenuates pain suppression by opioids and enhances the development of opioid tolerance and addiction, drug abuse, and other negative side effects such as respiratory depression and hyperalgesia. Drug candidates that target TLR4 may improve opioid-based pain management therapies.

Agonists

• Buprenorphine
• Carbamazepine
• Ethanol
• Fentanyl
• Levorphanol
• Lipopolysaccharides (LPS)
• Methadone
• Morphine
• Oxcarbazepine
• Oxycodone
• Pethidine

• Glucuronoxylomannan from Cryptococcus
• Morphine-3-glucuronide (inactive at opioid receptors, so selective for TLR4 activation)
• Tapentadol (mixed agonist/antagonist)
• "Unnatural" isomers such as (+)-morphine activate TLR4 but lack opioid receptor activity, although (+)-morphine also shows activity as a sigma receptor agonist.

Antagonists

• The lipid A analog eritoran acts as a TLR4 antagonist. As of December 2009, it was being developed as a drug against severe sepsis. However, in 2013, a news story said the results against sepsis were somewhat disappointing and that it was better used to treat certain cases of severe influenza. Although it does not treat the virus itself, it could be used against the massive immune reaction called cytokine storm which often occurs later in the infection and is a major cause of mortality from severe influenza.

• Amitriptyline
• Cyclobenzaprine
• Ketotifen
• Imipramine
• Mianserin
• Ibudilast
• Pinocembrin
• Naloxone
• Naltrexone
• (+)-naltrexone
• LPS-RS
• Propentofylline
• Tapentadol (mixed agonist/antagonist)

• (+)-naloxone ("unnatural" isomer, lacks opioid receptor affinity so selective for TLR4 inhibition)

External links

• Toll-Like Receptor 4 at the US National Library of Medicine Medical Subject Headings (MeSH)

UpToDate Contents

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• 1. 肥満細胞：表面受容体とシグナル伝達mast cells surface receptors and signal transduction [show details]
  …based on this mechanism have been reported . Toll-like receptor 4 (TLR4) also binds a protein produced by parasitic roundworms, ES-62 . Unlike the binding of TLR4 to lipopolysaccharide (LPS), however, ligation …
• 2. Toll様受容体：疾患および治療における役割toll like receptors roles in disease and therapy [show details]
  …TLR2/6, and TLR4) . There is also a MyD88-independent pathway via the molecule TIR domain-containing adapter-inducing interferon-beta (IFN-beta) (TRIF), which is used by TLR3 and TLR4 (TLR4 also utilizes …
• 3. 自然免疫系の概要an overview of the innate immune system [show details]
  … reward system in mice resulted in upregulation of innate immune cell receptors, including toll-like receptor 4 (TLR4), increased phagocytosis and killing of E. coli by macrophages, and an increased adaptive …
• 4. アテローム性動脈硬化症の病因pathogenesis of atherosclerosis [show details]
  …mRNAs. Further evidence for the role of inflammation comes from study of polymorphisms in the toll-like receptor 4 gene that confer differences in the inflammatory response to Gram negative pathogens and perhaps…
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  …lower levels of neutrophil Toll-like receptor 4 (TLR4) expression compared to age-matched controls . In mice, TLR4 controls the mucosal response to E. coli and inactivation of TLR4 can lead to a carrier state…

English Journal

• Apple polysaccharides induce apoptosis in colorectal cancer cells.

• Zhang D, Sun Y, Yue Z, Li Q, Meng J, Liu J, Hekong X, Jiang F, Mi M, Liu L, Mei Q.SourceDepartment of Pathogen Biology and Immunology, Xi'an Medical College, Xi'an 710021, Shaanxi, P.R. China.
• International journal of molecular medicine.Int J Mol Med.2012 Jul;30(1):100-6. doi: 10.3892/ijmm.2012.953. Epub 2012 Mar 26.
• Certain components of apples have been shown to prevent cancer growth and impede cancer progression. We hypothesized that extracted apple polysaccharides (APs) might, therefore, have anticancer effects, through a mechanism involving the induction of apoptosis in c
• PMID 22470124

• Foxp3 expression in A549 cells is regulated by Toll-like receptor 4 through nuclear factor-κB.

• Jia T, Fu H, Sun J, Zhang Y, Yang W, Li Y.SourceDepartment of Immunology, Norman Bethune College of Medicine, Jilin University, Changchun, Jilin 130021, P.R. China.
• Molecular medicine reports.Mol Med Report.2012 Jul;6(1):167-172. doi: 10.3892/mmr.2012.877. Epub 2012 Apr 18.
• Foxp3 is a master regulator of the development and function of CD4+CD25+ regulatory T cells (Tregs). Previous studies have reported that Foxp3 is also expressed in tumour cells and promotes tumour immune evasion. However, the regulation of the expression of Foxp3
• PMID 22576743

Japanese Journal

• Separation and characterization of the immunostimulatory components in unpolished rice black vinegar (kurozu)

• Hashimoto Masahito,Obara Kyoko,Ozono Mami [他]
• Journal of bioscience and bioengineering 116(6), 688-696, 2013-12
• NAID 40019929687

• プロスタグランジンE₂による自然免疫性炎症の抑制 (特集 自然免疫と炎症・自己免疫)

• 上田 真由美
• 臨床免疫・アレルギー科 60(6), 619-627, 2013-12
• NAID 40019921831

• TLR7の反応による自己免疫の誘導とGTPase (特集 自然免疫と炎症・自己免疫)

• 齋藤 伸一郎
• 臨床免疫・アレルギー科 60(6), 596-602, 2013-12
• NAID 40019921754

Related Pictures

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★リンクテーブル★

リンク元	「Toll様受容体4」「Toll様レセプター4」「TLR4」
関連記事	「like」「toll」

「Toll様受容体4」

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英

Toll-like receptor 4、TLR4

関

Toll様レセプター4

「Toll様レセプター4」

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英

Toll-like receptor 4

関

Toll様受容体4

「TLR4」

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• Toll様受容体4

関

Toll-like receptor 4

「like」

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• 好む

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• 似ている、同様の

関

alike、as well as、care for、correspond、correspondingly、equally、favor、identically、likewise、prefer、resemble、same、similar、similarly、such

　 　 　 　 　 　 　 　 　 　

「toll」

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• 料金

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