• 重慶醫(yī)科大學(xué)附屬第一醫(yī)院普外科（重慶400016）;

目的  綜述乳腺癌細(xì)胞逃避機體免疫監(jiān)視機理的研究進展。
方法  復(fù)習(xí)國內(nèi)、外相關(guān)文獻，從主要組織相容性抗原復(fù)合物（MHC）Ⅰ類分子表型改變、缺乏共刺激信號、腫瘤表達FasL、人類TNF相關(guān)凋亡誘導(dǎo)配體（TRAIL）的殺傷作用以及腫瘤抗原誘導(dǎo)機體免疫耐受幾個方面對乳腺癌免疫逃逸機理的研究進展加以綜述。
結(jié)果  MHCⅠ類分子表型改變,共刺激分子B7缺乏,腫瘤細(xì)胞表達FasL和TRAIL, 以及腫瘤抗原誘導(dǎo)機體免疫耐受與乳腺癌免疫逃逸有關(guān)。
結(jié)論  乳腺癌細(xì)胞通過自身抗原改變、不表達共刺激分子、誘導(dǎo)機體T淋巴細(xì)胞凋亡和機體免疫耐受而逃避機體免疫監(jiān)視，但對其免疫逃逸機理中各種因素的相互影響和綜合作用尚未被充分認(rèn)識。

引用本文： 孫正魁,姚榛祥. 乳腺癌免疫逃逸機理的研究進展. 中國普外基礎(chǔ)與臨床雜志, 2004, 11(1): 26-28. doi: 復(fù)制

1. Meazza R, Gaggero A, Neglia F, et al. Expression of two interleukin15 mRNA isoforms in human tumors does not correlate with secretion: role of different signal peptides [J]. Eur J Immunol, 1997; 27(5)∶1049.
2. Carosella ED, RouasFreiss N, Paul P, et al. HLAG: a tolerance molecule from the major histocompatibility complex [J]. Immunol Today, 1999; 20(2)∶60.
3. D’Orazio TJ, Niederkorn JY. A novel role for TGFbeta and IL10 in the induction of immune privilege [J]. J Immunol, 1998; 160(5)∶2089.
4. SalazarOnfray F. Interleukin10： a cytokine used by tumors to escape immunosurveillance [J]. Med Oncol, 1999; 16(2)∶86.
5. Chouaib S, AsselinPaturel C, MamiChouaib F, et al. The hosttumor immune conflict: from immunosuppression to resistance and destruction [J]. Immunol Today, 1997; 18(10)∶493.
6. Matsni S, Ahlers JD, Vortmeyer AO, et al. A model for CD8+ CTL tumor immunosurveillance and regulation of tumor escape by CD4 T cells through an effect on quality of CTL [J]. J Immunol, 1999; 163(1)∶184.
7. Adler AJ, Marsh DW, Yochum GS, et al. CD4+ T cell tolerance to parenchymal selfantigens requires presentation by bone marrowderived antigenpresenting cells [J]. J Exp Med, 1998; 187(10)∶1555.
8. O’Connell J, Bennett MW, O’Sullivan GC, et al. The Fas counterattack: cancer as a site of immune privilege [J]. Immunol Today, 1999; 20(1)∶46.
9. Zia A, Schildberg FM, Funke I. MHC classⅠnegative phenotype of disseminated tumor cells in bone marrow is associated with poor survival in ROMO breast cancer patients [J]. Int J Cancer, 2001; 93(4)∶566.
10. Feinmesser M, Sulkes A, Morgenstern S, et al. HLADR and beta 2 microglobulin expression in medullary and atypical medullary carcinoma of the breast: histopathologically similar but biologically distinct entities [J]. J Clin Pathol, 2000; 53(4)∶286.
11. Lefebvre S, Antoine M, Uzan S, et al. Specific activation of the nonclassical class Ⅰ histocompatibility HLAG antigen and expression of the ILT2 inhibitory receptor in human breast cancer [J]. J Pathol, 2002; 196(3)∶266.
12. Emtage PC, Wan Y, Bramson JL, et al. A double recombinant adenovirus expressing the costimulatory molecule B71 (murine) and human IL2 induces complete tumor regression in a murine breast adenocarcinoma model [J]. J Immunol, 1998; 160(5)∶2531.
13. Emtage PC, Wan Y, Muller W, et al. Enhanced interleukin2 gene transfer immunotherapy of breast cancer by coexpression of B71 and B72 [J]. J Interferon Cytokine Res, 1998; 18(11)∶927.
14. Giovarelli M, Musiani P, Garotta G, et al. A “stealth effect”: adenocarcinoma cells engineered to express TRAIL elude tumorspecific and allogeneic T cell reactions [J]. J Immunol, 1999; 163(9)∶4886.
15. Herrnring C, Reimer T, Jeschke U,et al. Expression of the apoptosisinducing ligands FasL and TRAIL in malignant and benign human breast tumors [J]. Histochem Cell Biol, 2000; 113(3)∶189.
16. O’Connell J, Bennett MW, O’Sullivan GC, et al. Expression of Fas (CD95/APO1) ligand by human breast cancers: significance for tumor immune privilege [J]. Clin Diagn Lab Immunol, 1999; 6(4)∶457.
17. Gutierrez LS, Eliza M, NivenFairchild T, et al. The Fas/Fasligand system: a mechanism for immune evasion in human breast carcinomas [J]. Breast Cancer Res Treat, 1999; 54(3)∶245.
18. Muschen M, Moers C, Warskulat U, et al. CD95 ligand expression in dedifferentiated breast cancer [J]. J Pathol, 1999; 189(3)∶378.
19. Muschen M, Moers C, Warskulat U, et al. CD95 ligand expression as a mechanism of immune escape in breast cancer [J]. Immunology, 2000; 99(1)∶69.
20. Kurt RA, Whitaker R, Baher A, et al. Spontaneous mammary carcinomas fail to induce an immune response in syngeneic FVBN202 neu transgenic mice [J]. Int J Cancer, 2000; 87(5)∶688.
  1. 1. Meazza R, Gaggero A, Neglia F, et al. Expression of two interleukin15 mRNA isoforms in human tumors does not correlate with secretion: role of different signal peptides [J]. Eur J Immunol, 1997; 27(5)∶1049.
  2. 2. Carosella ED, RouasFreiss N, Paul P, et al. HLAG: a tolerance molecule from the major histocompatibility complex [J]. Immunol Today, 1999; 20(2)∶60.
  3. 3. D’Orazio TJ, Niederkorn JY. A novel role for TGFbeta and IL10 in the induction of immune privilege [J]. J Immunol, 1998; 160(5)∶2089.
  4. 4. SalazarOnfray F. Interleukin10： a cytokine used by tumors to escape immunosurveillance [J]. Med Oncol, 1999; 16(2)∶86.
  5. 5. Chouaib S, AsselinPaturel C, MamiChouaib F, et al. The hosttumor immune conflict: from immunosuppression to resistance and destruction [J]. Immunol Today, 1997; 18(10)∶493.
  6. 6. Matsni S, Ahlers JD, Vortmeyer AO, et al. A model for CD8+ CTL tumor immunosurveillance and regulation of tumor escape by CD4 T cells through an effect on quality of CTL [J]. J Immunol, 1999; 163(1)∶184.
  7. 7. Adler AJ, Marsh DW, Yochum GS, et al. CD4+ T cell tolerance to parenchymal selfantigens requires presentation by bone marrowderived antigenpresenting cells [J]. J Exp Med, 1998; 187(10)∶1555.
  8. 8. O’Connell J, Bennett MW, O’Sullivan GC, et al. The Fas counterattack: cancer as a site of immune privilege [J]. Immunol Today, 1999; 20(1)∶46.
  9. 9. Zia A, Schildberg FM, Funke I. MHC classⅠnegative phenotype of disseminated tumor cells in bone marrow is associated with poor survival in ROMO breast cancer patients [J]. Int J Cancer, 2001; 93(4)∶566.
  10. 10. Feinmesser M, Sulkes A, Morgenstern S, et al. HLADR and beta 2 microglobulin expression in medullary and atypical medullary carcinoma of the breast: histopathologically similar but biologically distinct entities [J]. J Clin Pathol, 2000; 53(4)∶286.
  11. 11. Lefebvre S, Antoine M, Uzan S, et al. Specific activation of the nonclassical class Ⅰ histocompatibility HLAG antigen and expression of the ILT2 inhibitory receptor in human breast cancer [J]. J Pathol, 2002; 196(3)∶266.
  12. 12. Emtage PC, Wan Y, Bramson JL, et al. A double recombinant adenovirus expressing the costimulatory molecule B71 (murine) and human IL2 induces complete tumor regression in a murine breast adenocarcinoma model [J]. J Immunol, 1998; 160(5)∶2531.
  13. 13. Emtage PC, Wan Y, Muller W, et al. Enhanced interleukin2 gene transfer immunotherapy of breast cancer by coexpression of B71 and B72 [J]. J Interferon Cytokine Res, 1998; 18(11)∶927.
  14. 14. Giovarelli M, Musiani P, Garotta G, et al. A “stealth effect”: adenocarcinoma cells engineered to express TRAIL elude tumorspecific and allogeneic T cell reactions [J]. J Immunol, 1999; 163(9)∶4886.
  15. 15. Herrnring C, Reimer T, Jeschke U,et al. Expression of the apoptosisinducing ligands FasL and TRAIL in malignant and benign human breast tumors [J]. Histochem Cell Biol, 2000; 113(3)∶189.
  16. 16. O’Connell J, Bennett MW, O’Sullivan GC, et al. Expression of Fas (CD95/APO1) ligand by human breast cancers: significance for tumor immune privilege [J]. Clin Diagn Lab Immunol, 1999; 6(4)∶457.
  17. 17. Gutierrez LS, Eliza M, NivenFairchild T, et al. The Fas/Fasligand system: a mechanism for immune evasion in human breast carcinomas [J]. Breast Cancer Res Treat, 1999; 54(3)∶245.
  18. 18. Muschen M, Moers C, Warskulat U, et al. CD95 ligand expression in dedifferentiated breast cancer [J]. J Pathol, 1999; 189(3)∶378.
  19. 19. Muschen M, Moers C, Warskulat U, et al. CD95 ligand expression as a mechanism of immune escape in breast cancer [J]. Immunology, 2000; 99(1)∶69.
  20. 20. Kurt RA, Whitaker R, Baher A, et al. Spontaneous mammary carcinomas fail to induce an immune response in syngeneic FVBN202 neu transgenic mice [J]. Int J Cancer, 2000; 87(5)∶688.