prostate-specific antigen

前立腺特異抗原 PSA

WordNet

1. stated explicitly or in detail; "needed a specific amount"
2. a medicine that has a mitigating effect on a specific disease; "quinine is a specific for malaria"
3. (sometimes followed by `to'
4. being or affecting a disease produced by a particular microorganism or condition; used also of stains or dyes used in making microscope slides; "quinine is highly specific for malaria"; "a specific remedy"; "a specific stain is one having a specific affinity for particular structural elements"
5. relating to or distinguishing or constituting a taxonomic species; "specific characters"
6. any substance (as a toxin or enzyme) that stimulates an immune response in the body (especially the production of antibodies)
7. relating to the prostate gland (同)prostatic

PrepTutorEJDIC

1. 《名詞の前にのみ用いて》『特定の』,一定の・『明確な』,明白な・(そのものに)『特有の』,独特の《+『to』+『名』》・〈C〉(…の)特効薬《+『for』+『名』》・《複数形で》明細,細部(details)
2. 抗原(生物の体内にはいって免疫体を作る物質)
3. 前立腺(せん)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/12/22 22:54:44」(JST)

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Kallikrein related peptidase 3
Crystallographic structure of human prostate-specific antigen (green/gold cartoon) covalently attached to an substrate acyl intermediate (multicolor sticks, carbon = white, nitrogen = blue, oxygen = red) and an glucosamine–manose disaccharide (spheres, carbon = yellow and oxygen = red).
Available structures PDB Ortholog search: PDBe, RCSB List of PDB id codes 1PFA, 2PSA, 2ZCH, 2ZCK, 2ZCL, 3QUM
Identifiers
Symbols	KLK3 ; APS; KLK2A1; PSA; hK3
External IDs	OMIM: 176820 MGI: 892021 HomoloGene: 68141 ChEMBL: 2099 GeneCards: KLK3 Gene
EC number	3.4.21.77
Gene ontology Molecular function • endopeptidase activity • serine-type endopeptidase activity • protein binding • serine-type peptidase activity • hydrolase activity, acting on carbon-nitrogen (but not peptide) bonds, in linear amides Cellular component • extracellular region • extracellular space • nucleus • protein complex • extracellular exosome Biological process • antibacterial peptide production • proteolysis • small GTPase mediated signal transduction • negative regulation of angiogenesis • cellular protein metabolic process Sources: Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	354	13646
Ensembl	ENSG00000142515	ENSMUSG00000060177
UniProt	P07288	P15948
RefSeq (mRNA)	NM_001030047	NM_010114
RefSeq (protein)	NP_001025218	NP_034244
Location (UCSC)	Chr 19: 50.85 – 50.86 Mb	Chr 7: 44.11 – 44.12 Mb
PubMed search	[1]	[2]

Prostate-specific antigen (PSA), also known as gamma-seminoprotein or kallikrein-3 (KLK3), is a glycoprotein enzyme encoded in humans by the KLK3 gene. PSA is a member of the kallikrein-related peptidase family and is secreted by the epithelial cells of the prostate gland. PSA is produced for the ejaculate, where it liquefies semen in the seminal coagulum and allows sperm to swim freely. It is also believed to be instrumental in dissolving cervical mucus, allowing the entry of sperm into the uterus.

PSA is present in small quantities in the serum of men with healthy prostates, but is often elevated in the presence of prostate cancer or other prostate disorders. The United States Preventive Services Task Force (USPSTF, 2012) does not recommend PSA screening for prostate cancer, noting that the test may result in “overdiagnosis” and “overtreatment” because "most prostate cancer is asymptomatic for life" and treatments involve risks of complications including impotence (erectile dysfunction) and incontinence. The USPSTF concludes "the potential benefit does not outweigh the expected harms." PSA is not a unique indicator of prostate cancer, but may also detect prostatitis or benign prostatic hyperplasia. 30 percent of patients with high PSA have prostate cancer diagnosed after biopsy.

Medical uses

Prostate cancer

Screening

Main article: Prostate cancer screening

Clinical practice guidelines for prostate cancer screening vary and are controversial due to uncertainty as to whether the benefits of screening ultimately outweigh the risks of overdiagnosis and over treatment. In the United States, the U.S. Food and Drug Administration (FDA) has approved the PSA test for annual screening of prostate cancer in men of age 50 and older. The patient needs to be informed of the risks and benefits of PSA testing prior to performing the test (see below). PSA levels between 4 and 10 ng/mL (nanograms per milliliter) are considered to be suspicious and consideration should be given to confirming the abnormal PSA with a repeat test. If indicated, prostate biopsy is performed to obtain tissue sample for histopathological analysis. In the United Kingdom, the National Health Service (2005) does not mandate, nor advise for PSA test, but allows patients to decide based on their doctor's advice.

A review commissioned by the U.S. Preventive Services Task Force concluded that "Prostate-specific antigen-based screening results in small or no reduction in prostate cancer-specific mortality and is associated with harms related to subsequent evaluation and treatments, some of which may be unnecessary," or more simply, "[t]he potential benefit does not outweigh the expected harms" in patients not already diagnosed or being treated for prostate cancer.

While PSA testing may help 1000 in 1,000,000 avoid death due to prostate cancer, 4000 to 5000 in 1,000,000 would die from prostate cancer after 10 years even with screening. This means that PSA screening may reduce mortality from prostate cancer by up to 25%. Expected harms include anxiety for 100 – 120 receiving false positives, biopsy pain, and other complications from biopsy for false positive tests. Of those found to have prostate cancer, frequent overdiagnosis is common because most cases of prostate cancer are not expected to cause any symptoms. Therefore many will experience the side effects of treatment, such as for every 100 men screened, 2.9 will experience erectile dysfunction, 1.8 will suffer urinary incontinence, .2 will have serious cardiovascular events, .1 will suffer pulmonary embolus or deep venous thrombosis, and .1 perioperative death. Since the expected harm relative to risk of death are perceived by patients as minimal, men found to have prostate cancer usually (up to 90% of cases) select to receive treatment.

Risk stratification and staging

Men with prostate cancer may be characterized as low-, intermediate-, or high-risk for having/developing metastatic disease or dying of prostate cancer. PSA level is one of three variables on which the risk-stratification is based; the others are the grade of prostate cancer (Gleason grading system) and the stage of cancer based on physical examination and imaging studies. Criteria for each risk category are as follows:

Low-risk: PSA < 10, Gleason score ≤ 6, AND clinical stage ≤ T2a

Intermediate-risk: PSA 10-20, Gleason score 7, OR clinical stage T2b/c

High-risk: PSA > 20, Gleason score ≥ 8, OR clinical stage ≥ T3

Post-treatment monitoring

PSA levels are monitored periodically (e.g., every 6–36 months) after treatment for prostate cancer - more frequently in patients with high-risk disease, less frequently in patients with lower-risk disease. If surgical therapy (i.e., radical prostatectomy) is successful at removing all prostate tissue (and prostate cancer), PSA becomes undetectable within a few weeks. A subsequent rise in PSA level above 0.2 ng/mL L is generally regarded as evidence of recurrent prostate cancer after a radical prostatectomy; less commonly, it may simply indicate residual benign prostate tissue.

Following radiation therapy of any type for prostate cancer, some PSA levels might be detected, even when the treatment ultimately proves to be successful. This makes it more difficult to interpret the relationship between PSA levels and recurrence/persistence of prostate cancer after radiation therapy. PSA levels may continue to decrease for several years after radiation therapy. The lowest level is referred to as the PSA nadir. A subsequent increase in PSA levels by 2.0 ng/dL above the nadir is the currently accepted definition of prostate cancer recurrence after radiation therapy.

If recurrent prostate cancer is detected by a rise in PSA levels after curative treatment, it is referred to as a "biochemical recurrence". The likelihood of developing recurrent prostate cancer after curative treatment is related to the pre-operative variables described in the preceding section (PSA level and grade/stage of cancer). Low-risk cancers are the least likely to recur, but they are also the least likely to have required treatment in the first place.

Histology

PSA is produced in the epithelial cells of the prostate, and can be demonstrated in biopsy samples or other histological specimens using immunohistochemistry. Disruption of this epithelium, for example in inflammation or benign prostatic hyperplasia, may lead to some diffusion of the antigen into the tissue around the epithelium, and is the cause of elevated blood levels of PSA in these conditions.

More significantly, PSA remains present in prostate cells after they become malignant. Prostate cancer cells generally have variable or weak staining for PSA, due to the disruption of their normal functioning. Thus, individual prostate cancer cells produce less PSA than healthy cells; the raised serum levels in prostate cancer patients is due to the greatly increased number of such cells, not their individual activity. However, in most cases of prostate cancer, the cells remain positive for the antigen, which can therefore be used to identify metastasis. Since some high-grade prostate cancers may be entirely negative for PSA, however, histological analysis to identify such cases usually uses PSA in combination with other antibodies, such as PSAP and CD57.

Forensic identification of semen

PSA was first identified by researchers attempting to find a substance in seminal fluid that would aid in the investigation of rape cases. PSA is now used to indicate the presence of semen in forensic serology. The semen of adult males has PSA levels far in excess of those found in other tissues; therefore, a high level of PSA found in a sample is an indicator that semen may be present. Because PSA is a biomarker that is expressed independently of spermatozoa, it remains useful in identifying semen from vasectomized and azoospermic males.

PSA can also be found at low levels in other body fluids, such as urine and breast milk, thus setting a high minimum threshold of interpretation to rule out false positive results and conclusively state that semen is present. While traditional tests such as crossover electrophoresis have a sufficiently low sensitivity to detect only seminal PSA, newer diagnostics tests developed from clinical prostate cancer screening methods have lowered the threshold of detection down to 4 ng/mL. This level of antigen has been shown to be present in the peripheral blood of males with prostate cancer, and rarely in female urine samples and breast milk. No studies have been performed to assess the PSA levels in the tissues and secretions of pre-pubescent children. Therefore, the presence of PSA from a high sensitivity (4 ng/mL) test cannot conclusively identify the presence of semen, so care must be taken with the interpretation of such results.

Mechanism of action

The physiological function of KLK3 is the dissolution of the coagulum, the sperm entrapping gel composed of semenogelins and fibronectin. Its proteolic action is effective in liquefying the coagulum so that the sperm can be liberated. The activity of PSA is well regulated. In the prostate it is present as an inactive pro-form which is activated through the action of KLK2, another kallikrein-related peptidase. In the prostate, zinc ion concentrations are ten times higher than in other bodily fluids. Zinc ions have a strong inhibitory effect on the activity of PSA and on that of KLK2, so that PSA is totally inactive. Further regulation is achieved through pH variations. Although its activity is increased by higher pH, the inhibitory effect of zinc also increases. The pH of semen is slightly alkaline and the concentrations of zinc are high. On ejaculation, semen is exposed to the acidic pH of the vagina, due to the presence of lactic acid. In fertile couples, the final vaginal pH after coitus approaches the 6-7 levels, which coincides well with reduced zinc inhibition of PSA. At these pH levels, the reduced PSA activity is countered by a decrease in zinc inhibition. Thus, the coagulum is slowly liquefied, releasing the sperm in a well regulated manner.

Biochemistry

Prostate-specific antigen (PSA, also known as kallikrein III, seminin, semenogelase, γ-seminoprotein and P-30 antigen) is a 34-kD glycoprotein produced almost exclusively by the prostate gland. It is a serine protease (EC 3.4.21.77) enzyme, the gene of which is located on the 19th chromosome (19q13) in humans.

History

The discovery of prostate-specific antigen (PSA) is beset with controversy; as PSA is present in prostatic tissue and semen, it was independently discovered and given different names, thus adding to the controversy.

Flocks was the first to experiment with antigens in the prostate and 10 years later Albin reported the presence of precipitation antigens in the prostate.

In 1971, Hara characterized a unique protein in the semen fluid, gamma-seminoprotein. Li and Beling, in 1973, isolated a protein, E1, from human semen in an attempt to find a novel method to achieve fertility control.

In 1978, Sensabaugh identified semen-specific protein p30, but proved that it was similar to E1 protein, and that prostate was the source. In 1979, Wang purified a tissue-specific antigen from the prostate ('prostate antigen').

PSA was first measured quantitatively in the blood by Papsidero in 1980, and Stamey carried out the initial work on the clinical use of PSA as a marker of prostate cancer.

Serum levels

PSA is normally present in the blood at very low levels. The reference range of less than 4 ng/mL for the first commercial PSA test, the Hybritech Tandem-R PSA test released in February 1986, was based on a study that found 99% of 472 apparently healthy men had a total PSA level below 4 ng/mL—the upper limit of normal is much less than 4 ng/mL.

Increased levels of PSA may suggest the presence of prostate cancer. However, prostate cancer can also be present in the complete absence of an elevated PSA level, in which case the test result would be a false negative.

Obesity has been reported to reduce serum PSA levels. Delayed early detection may partially explain worse outcomes in obese men with early prostate cancer. After treatment, higher BMI also correlates to higher risk of recurrence.

PSA levels can be also increased by prostatitis, irritation, benign prostatic hyperplasia (BPH), and recent ejaculation, producing a false positive result. Digital rectal examination (DRE) has been shown in several studies to produce an increase in PSA. However, the effect is clinically insignificant, since DRE causes the most substantial increases in patients with PSA levels already elevated over 4.0 ng/mL.

The "normal" reference ranges for prostate-specific antigen increase with age, as do the usual ranges in cancer:

Age	<50		50 - 59		60 - 69		>70		(years)
	Cancer	No cancer	Cancer	No cancer	Cancer	No cancer	Cancer	No cancer
5th percentile	0.4	0.3	1.2	0.3	1.7	0.3	2.3	0.4	(ng/mL)
95th percentile	163.0	2.5	372.5	4.7	253.2	8.3	613.2	17.8

PSA velocity

Risk of prostate cancer in two age groups based on Free PSA as % of Total PSA

Despite earlier findings, recent research suggests that the rate of increase of PSA (e.g. >0.35 ng/mL/yr, the 'PSA velocity') is not a more specific marker for prostate cancer than the serum level of PSA.

However, the PSA rate of rise may have value in prostate cancer prognosis. Men with prostate cancer whose PSA level increased by more than 2.0 ng per milliliter during the year before the diagnosis of prostate cancer have a higher risk of death from prostate cancer despite undergoing radical prostatectomy. PSA velocity (PSAV) was found in a 2008 study to be more useful than the PSA doubling time (PSA DT) to help identify those men with life-threatening disease before start of treatment.

Free PSA

Most PSA in the blood is bound to serum proteins. A small amount is not protein bound and is called 'free PSA'. In men with prostate cancer the ratio of free (unbound) PSA to total PSA is decreased. The risk of cancer increases if the free to total ratio is less than 25%. (See graph at right.) The lower the ratio is, the greater the probability of prostate cancer. Measuring the ratio of free to total PSA appears to be particularly promising for eliminating unnecessary biopsies in men with PSA levels between 4 and 10 ng/mL. However, both total and free PSA increase immediately after ejaculation, returning slowly to baseline levels within 24 hours.

Inactive PSA

The PSA test in 1994 failed to differentiate between prostate cancer and benign prostate hyperplasia (BPH) and the commercial assay kits for PSA did not provide correct PSA values. Thus with the introduction of the ratio of free to total PSA, the reliability of the test has improved and measuring the activity of the enzyme could add to the ratio of free to total PSA and further improve the diagnostic value of test. Proteolytically active PSA has been shown to have an anti-angiogenic effect and certain inactive subforms may be associated with prostate cancer, as shown by MAb 5D3D11, an antibody able to detect forms abundantly represented in sera from cancer patients. The presence of inactive proenzyme forms of PSA is another potential indicator of disease.

PSA in other biologic fluids and tissues

Concentration of PSA in human body fluids

Fluid	PSA (ng/mL)
semen	200,000 - 5.5 million
amniotic fluid	0.60 - 8.98
breast milk	0.47 - 100
saliva	0
female urine	0.12 - 3.72
female serum	0.01 - 0.53

It is now clear that the term prostate-specific antigen is a misnomer: it is an antigen but is not specific to the prostate. Although present in large amounts in prostatic tissue and semen, it has been detected in other body fluids and tissues.

In women, PSA is found in female ejaculate at concentrations roughly equal to that found in male semen. Other than semen and female ejaculate, the greatest concentrations of PSA in biological fluids are detected in breast milk and amniotic fluid. Low concentrations of PSA have been identified in the urethral glands, endometrium, normal breast tissue and salivary gland tissue. PSA also is found in the serum of women with breast, lung, or uterine cancer and in some patients with renal cancer.

Tissue samples can be stained for the presence of PSA in order to determine the origin of malignant cells that have metastasized.

Interactions

Prostate-specific antigen has been shown to interact with protein C inhibitor.

See also

• Tumor markers

References

Further reading

• De Angelis G, Rittenhouse HG, Mikolajczyk SD, Blair Shamel L, Semjonow A (2007). "Twenty Years of PSA: From Prostate Antigen to Tumor Marker". Reviews in Urology 9 (3): 113–23. PMC 2002501. PMID 17934568. 
• Henttu P, Vihko P (Jun 1994). "Prostate-specific antigen and human glandular kallikrein: two kallikreins of the human prostate". Annals of Medicine 26 (3): 157–64. doi:10.3109/07853899409147884. PMID 7521173. 
• Diamandis EP, Yousef GM, Luo LY, Magklara A, Obiezu CV (Mar 2000). "The new human kallikrein gene family: implications in carcinogenesis". Trends in Endocrinology and Metabolism 11 (2): 54–60. doi:10.1016/S1043-2760(99)00225-8. PMID 10675891. 
• Lilja H (Nov 2003). "Biology of prostate-specific antigen". Urology 62 (5 Suppl 1): 27–33. doi:10.1016/S0090-4295(03)00775-1. PMID 14607215. 

External links

• The MEROPS online database for peptidases and their inhibitors: S01.162
• American Cancer Society: Detailed Guide: Prostate Cancer Can Prostate Cancer Be Found Early?
• National Cancer Institute: The Prostate-Specific Antigen (PSA) Test: Questions and Answers
• Prostate-Specific Antigen at the US National Library of Medicine Medical Subject Headings (MeSH)
• Prostate UK Help us stop prostate diseases ruining lives
• PSA at Lab Tests Online

UpToDate Contents

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• 1. 前立腺特異的抗原（PSA）の測定 measurement of prostate specific antigen
• 2. 前立腺癌のスクリーニング screening for prostate cancer
• 3. 前立腺癌に対する局所療法に伴う血清PSAの上昇：定義、自然経過、およびリスク層別化 rising serum psa following local therapy for prostate cancer definition natural history and risk stratification
• 4. 前立腺癌治療中および治療後のフォローアップにおけるサーベイランス follow up surveillance during and after treatment for prostate cancer
• 5. 前立腺癌に対する局所療法に伴う血清PSAの上昇：診断評価 rising serum psa following local therapy for prostate cancer diagnostic evaluation

English Journal

• Wild-type and specific mutant androgen receptor mediates transcription via 17β-estradiol in sex hormone-sensitive cancer cells.

• Susa T1, Ikaga R, Kajitani T, Iizuka M, Okinaga H, Tamamori-Adachi M, Okazaki T.
• Journal of cellular physiology.J Cell Physiol.2015 Jul;230(7):1594-606. doi: 10.1002/jcp.24906.
• We previously encountered regulatory processes wherein dihydrotestosterone (DHT) exerted its inhibitory effect on parathyroid hormone-related protein (PTHrP) gene repression through the estrogen receptor (ER)α, but not the androgen receptor (AR), in breast cancer MCF-7 cells. Here, we investigated
• PMID 25536295

• Label-free electrochemical detection of prostate-specific antigen based on nucleic acid aptamer.

• Souada M1, Piro B2, Reisberg S1, Anquetin G1, Noël V1, Pham MC1.
• Biosensors & bioelectronics.Biosens Bioelectron.2015 Jun 15;68:49-54. doi: 10.1016/j.bios.2014.12.033. Epub 2014 Dec 16.
• We report a label-free aptasensor to make direct detection of prostate specific antigen (PSA, a biomarker of prostate cancer) using a quinone-containing conducting copolymer acting as redox transducer and grafting matrix for immobilization of the short aptamer strands. It is shown that capture of PS
• PMID 25569871

• Androgens and obesity in male adolescents.

• Vandewalle S1, De Schepper J, Kaufman JM.
• Current opinion in endocrinology, diabetes, and obesity.Curr Opin Endocrinol Diabetes Obes.2015 Jun;22(3):230-7. doi: 10.1097/MED.0000000000000160.
• PURPOSE OF REVIEW: Data on sex steroid levels and pubertal development in obese adolescent boys are scarce and contrasting. The present review summarizes the most recent results obtained with improved methodology to measure low sex steroid levels in children.RECENT FINDINGS: Obese pubertal boys have
• PMID 25871956

Japanese Journal

• Understanding prostate-specific antigen dynamics in monitoring metastatic castration-resistant prostate cancer: implications for clinical practice

• Asian journal of andrology 19(2), 143-148, 2017-03-01
• NAID 120006226801

• 前立腺肥大症患者の前立腺癌罹患リスク

• 日本保険医学会誌 = Japanese journal of insurance medicine 115(1), 36-42, 2017-03
• NAID 40021170549

• Clinical and histopathological characteristics of patients with prostate cancer in the BioBank Japan project

• Journal of epidemiology 27(3), S65-S70, 2017-03
• NAID 120006219868

Related Links

• Prostate-specific antigen - Wikipedia, the free encyclopedia

Prostate-specific antigen (PSA), also known as gamma-seminoprotein or kallikrein-3 (KLK3), is a glycoprotein encoded in humans by the KLK3 gene. PSA is a member of the kallikrein-related peptidase family and is secreted by the epithelial ...

Related Pictures

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★リンクテーブル★

リンク元	「前立腺特異抗原」「PSA」
関連記事	「specific」「specific antigen」

「前立腺特異抗原」

　　[★]

英

prostate specific antigen, prostate-specific antigen, PSA, PA

関

前立腺、前立腺液、前立腺癌。PAP

概念

LAB.639 OLM.377

• 前立腺上皮細胞から分泌されるキニン-カリクレインファミリーに属する分子量33～34kDaの糖蛋白で、セリンプロテアーゼの一種である。
• 精液中に含まれ、精子運動性の亢進および精漿の液状化に関与するといわれている。
• 一部血中に逸脱するため、血清PSAとして測定することができる。
• 血液中では10-20%がfree PSAとして存在するが、多くはα1-アンチキモトリプシン(ACT)と結合している。
• 前立腺癌では総PSAに対するACT-PSA複合体の割合が増加するため、前立腺肥大症との鑑別に有用かもしれない。
• 前立腺癌の診断や治療経過をみる腫瘍マーカーとして用いられているが、生理的、あるいは他の疾患でも上昇することがある。
• Tandem-Rキットでの基準値が臨床では良く用いられている、らしい。(ガイドラインにも記載があった気がした)

判定

• 正常：4ng/ml以下(IRMA法) (参考1)
• グレーゾーン：4-10 ng/ml
• 高値：10ng/ml

LAB.640

• 加齢により増加するため、年齢階層別基準値が定められている。

高値

LAB.639 OLM.377

• 前立腺癌：腫瘍量とPSAとは正の相関関係にある。
• 前立腺肥大症：PSA軽度上昇を示す。確定診断には前立腺生検が必要　　←　　そこまでする？？？
• 尿路・前立腺の炎症：急性前立腺炎
• 機械的刺激：長時間のサイクリング、前立腺マッサージ、前立腺生検、尿道カテーテル留置、膀胱鏡検査、前立腺手術
• その他：急性尿閉、射精後

臨床的意義

• 前立腺癌、前立腺肥大症、前立腺炎などで上昇。PSAのみではこれらの鑑別はできない。

注意

• フィナステリド服用例ではPSAの値に影響を与える可能性がある。
• 前立腺肥大症に対するステロイド系抗アンドロゲン薬服用例ではPSAに影響を与える可能性がある。

参考

• 1. 体外診断用放射性医薬品/タンデム-R free PSA

http://www.yamasa.com/shindan/seihin/freePSA/freepsa.htm#rinsyou

「PSA」

　　[★] 前立腺特異抗原 prostate-specific antigen

「specific」

　　[★]

• adj.

• (～に関して)明確な、はっきりとした(exact precise)、具体的な(in, about)
• (比較)(限定)特定の(particular)、一定の(⇔general)
• (～に)特有の、独特の(to)
• (比較)(医学)(～に)渡航のある(for)。特殊な
• (生物)(生物)種の
• 医学)特異の
• (物理)比の。物質固有の。単位質量・長さ・面積・容積で

n.

関

specifically、specificity

　 　 　 　 　 　

「specific antigen」

　　[★]

• 特異抗原、特異的抗原