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1
B lymphocyte immune response gene phenotype is genetically determined.
J Exp Med. 1982 Apr 1;155(4):1239-44. doi: 10.1084/jem.155.4.1239.
2
Gene complementation. Neither Ir-GLphi gene need be present in the proliferative T cell to generate an immune response to Poly(Glu55Lys36Phe9)n.
J Exp Med. 1980 Jun 1;151(6):1452-67. doi: 10.1084/jem.151.6.1452.
3
Inhibition of antigen-induced proliferation of T cells from radiation-induced bone marrow chimeras by a monoclonal antibody directed against an Ia determinant on the antigen-presenting cell.
Proc Natl Acad Sci U S A. 1981 Jan;78(1):514-8. doi: 10.1073/pnas.78.1.514.
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T lymphocyte-dependent B lymphocyte proliferative response to antigen. I Genetic restriction of the stimulation of B lymphocyte proliferation.
J Exp Med. 1981 Apr 1;153(4):871-82. doi: 10.1084/jem.153.4.871.
6
Gene complementation in the T-lymphocyte proliferative response to poly (Glu55Lys36Phe9)n. A demonstration that both immune response gene products must be expressed in the same antigen-presenting cell.
J Exp Med. 1979 Jan 1;149(1):40-57. doi: 10.1084/jem.149.1.40.
7
The involvement of suppressor T cells in Ir gene regulation of secondary antibody responses of primed (responder X nonresponder)F1 mice to macrophage-bound L-glutamic acid60-L-alanine30-L-tyrosine.
J Exp Med. 1978 Nov 1;148(5):1324-37. doi: 10.1084/jem.148.5.1324.
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9
T cell subsets in (responder x nonresponder)F1 mice regulating antibody responses to L-glutamic acid60-L-alanine30-L-tyrosine (GAT).
J Immunol. 1984 Dec;133(6):2874-81.
10
Antigen presentation in the murine T lymphocyte proliferative response. II. Ir-GAT-controlled T lymphocyte responses require antigen-presenting cells from a high responder donor.
Eur J Immunol. 1978 May;8(5):344-7. doi: 10.1002/eji.1830080510.
本文引用的文献
1
Antigen recognition. V. Requirement for histocompatibility between antigen-presenting cell and B cell in the response to a thymus-dependent antigen, and lack of allogeneic restriction between T and B cells.
J Exp Med. 1981 Sep 1;154(3):676-87. doi: 10.1084/jem.154.3.676.
2
Selective loss of antigen-specific Ir gene function in IA mutant B6.C-H-2bm12 is an antigen presenting cell defect.
Proc Natl Acad Sci U S A. 1981 Oct;78(10):6406-10. doi: 10.1073/pnas.78.10.6406.
3
T lymphocyte-dependent B lymphocyte proliferative response to antigen. I Genetic restriction of the stimulation of B lymphocyte proliferation.
J Exp Med. 1981 Apr 1;153(4):871-82. doi: 10.1084/jem.153.4.871.
4
Inhibition of antigen-induced proliferation of T cells from radiation-induced bone marrow chimeras by a monoclonal antibody directed against an Ia determinant on the antigen-presenting cell.
Proc Natl Acad Sci U S A. 1981 Jan;78(1):514-8. doi: 10.1073/pnas.78.1.514.
5
Monoclonal antibody against an Ir gene product?
J Exp Med. 1980 Oct 1;152(4):1085-101. doi: 10.1084/jem.152.4.1085.
6
Cell interactions between histoincompatible T and B lymphocytes. VII. Cooperative responses between lymphocytes are controlled by genes in the I region of the H-2 complex.
J Exp Med. 1975 Jan 1;141(1):263-8. doi: 10.1084/jem.141.1.263.
7
Lymphoid function in F1 leads to parent chimeras: lack of evidence for adaptive differentiation of B cells or antigen-presenting cells.
J Exp Med. 1979 Sep 19;150(3):715-20. doi: 10.1084/jem.150.3.715.
8
H-2 antigens of the thymus determine lymphocyte specificity.
J Exp Med. 1978 Sep 1;148(3):766-75. doi: 10.1084/jem.148.3.766.
9
Adaptive differentiation of murine lymphocytes. I. Both T and B lymphocytes differentiating in F1 transplanted to parental chimeras manifest preferential cooperative activity for partner lymphocytes derived from the same parental type corresponding to the chimeric host.
J Exp Med. 1978 Sep 1;148(3):727-45. doi: 10.1084/jem.148.3.727.
10
Restricted helper function of F1 leads to parent bone marrow chimeras controlled by K-end of H-2 complex.
J Exp Med. 1978 Jun 1;147(6):1838-42. doi: 10.1084/jem.147.6.1838.
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