1987 Fiscal Year Final Research Report Summary
ANALYSIS OF REGULATION MECHANISMS OF T CELL REPERTORY IN RECOGNITION OF MHC CLASS II
| Project/Area Number |
61570237
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | SHINSHU UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
YANO A. DEPARTMENT OF PARASITOLOGY, 医学部, 講師 (20135122)
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| Project Period (FY) |
1986 – 1987
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| Keywords | APC / MHC molecule / Non-MHC molecule / CIM-1 molecule / T cell activation / D2A2 mAb / T細胞レパートリー統御 |
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| Research Abstract |
TWO MOCLONAL ANTIBODIES,IAb1 AND D2A2 mAbs,WERE ESTABLISHED BY THE CELL FUSION OF P3U1 AND T@e sPLEEN CELLS FROM BALB/C MOUSE IMMUNIZED WITH HUMAN B LYMPHOMA, ARH-8AZ. THE ANTIBODIES ARE CROSS-REACTIVE WITH NOT ONLY HUMAN HLA-@r BUT ALSO CLASS IT OF OTHER VERTEBRATES. THE MONOCLONAL ANTIBODIES SHOWED TO HAVE DIFFRENT INHIBITORY EFFECT BETWEEN B6 AND BALB.B MICE IN ANTIGEN-SPECIFIC T CELL ACTIVATION.ANTIGEN-SPECIFIC T CELL RESPONSES WERE BLOCKED BY BOTH IAb1 BUT NOT BY D2A2, WHEREAS THOSE OF BALB.B WERE BLOCKED BY BOTH IAb1 AND D2A2. THE DIFFERENT BLOCKING EFFECT OF D2A2 BETWEEN B6 AND BALB.B IS ACCOUNTED FOR BY APC LEVEL BUT NOT BY T CELL REPERTORIES, BECAUSE ANTIGEN-SPECIFIC PROLIFERATIVE RESPONSES OF (B6xBALB.B)F1 T CELLS STIMULATED BY BALB.B APC BUT NOT BY B6 APC WERE BLOCKED BY D2A2. THE CHIMERIC EXPERIMENT USING B10 Thy 1.1 AND BALB.B Thy 1.2 MICE REVEALED THAT THE LIABILITY OF T CELL RESPONSE INHIOBITION BY D2A2 WAS DEPENDENT UPON DEVELOPMENTAL ENVIRONMENT OF T CELLS. IN ORDER TO INVESTIGATE NON-H-2 MOLECULE, SD RAT WAS IMMUNIZED WITH MURIN MACROPHAGE CELL LINE, P388D1, AND A MONOCLONAL ANTIBODY(CIM-1) WAS ESTABLISHED. CIM-1 mAb PRECIPITATED 35K,60K NON-COVALENTLY BOUND PEPTIDE OF P388D1. THIS NON-H-2 MOLECULE WAS SHOWN TO FUNCTION IN THE CELL INTERACRION BETWEEN SYNGENEIC, ALLOGENEIC AND XENOGENEIC APC-T CELLS. THE MOLECULE ALSO PLAYED A ROLE IN THE THYMOCYTE PROLIFERATIVE RESPONSE TO IL-1 AND LECTIN. THUS, NOT ONLYH-2 BUT ALSO NON-H-2(CIM-1) ARE PARTICIPATING IN ANTIGEN-SPECTFIC ACTIVATION OF T CELLS BY ApC AND IN REGULATION OF T CELL REPERTORIES.
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