Thymic immune response gene function in radiation chimeras reconstituted with purified hemopoietic stem cells

Immune response (Ir) genes are encoded for by the I region of the major histocompatibility complex (MHC). A class of serologically defined specificities, Ia antigens, is also encoded for by genes within this region. A new Ia specificity, Ia.W39, has recently been defined. It is private for I-Ab and its expression is controlled by a gene on the X-chromosome. Using different approaches, the role of Ia.W39 in the immune response of H-2b mice to beef insulin was examined in a macrophage-dependent T cell proliferation assay. It was found that beef insulin-related Ir gene function was associated with the expression of Ia.W39 by antigen-presenting macrophages and that control of this Ir gene function was X-linked (xid gene).

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DETERMINANT SELECTION: A MACROPHAGE-MEDIATED IMMUNE RESPONSE GENE FUNCTION

Ir Genes and Ia Antigens ◽

10.1016/b978-0-12-483260-2.50048-3 ◽

1978 ◽

pp. 405-415 ◽

Cited By ~ 2

Author(s):

Alan S. Rosenthal ◽

Lanny J. Rosenwasser ◽

Marcello A. Barcinski

Keyword(s):

Immune Response ◽

Gene Function ◽

Immune Response Gene ◽

Response Gene

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Antigen-presenting cells from nonresponder strain 2 guinea pigs are fully competent to present bovine insulin B chain to responder strain 13 T cells. Evidence against a determinant selection model and in favor of a clonal deletion model of immune response gene function.

Journal of Experimental Medicine ◽

10.1084/jem.157.4.1287 ◽

1983 ◽

Vol 157 (4) ◽

pp. 1287-1299 ◽

Cited By ~ 32

Author(s):

G A Dos Reis ◽

E M Shevach

Keyword(s):

Immune Response ◽

T Cells ◽

Gene Function ◽

Guinea Pigs ◽

Bovine Insulin ◽

Immune Response Gene ◽

Cell Repertoire ◽

Clonal Deletion ◽

Response Gene ◽

Selection Hypothesis

To test directly the determinant selection hypothesis of immune response gene function, we primed strain 13 T lymphocytes in vitro with allogeneic bovine insulin pulsed strain 2 macrophages. Strain 2 macrophages were found to be fully competent to present bovine insulin B chain to strain 13 T cells despite the fact that strain 2 guinea pigs are normally totally unresponsive to this antigen. These results are incompatible with a strict interpretation of the determinant selection hypothesis, which would have predicted that strain 2 macrophages would have been restricted to the presentation of A chain loop determinants. In addition, a comparison of the reactivity profiles of self-Ia- and allo-Ia-restricted strain 13 T cells to a series of synthetic B chain peptide fragments revealed that the allo-Ia-restricted populations could be activated by autologous guinea pig insulin. Taken together, these observations strongly suggest that the clonal deletion of self-reactive cells is likely to be I region restricted and that nonresponsiveness to any protein antigen may result from a restriction in the T cell repertoire that is generated during ontogeny by a clonal deletion mechanism of tolerance to self.

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The XID gene controls Ia.W39 associated immune response gene function for insulin induced T cell activation

Basic and clinical aspects of immunity to insulin ◽

10.1515/9783111518053-011 ◽

1981 ◽

pp. 105-114

Author(s):

L. J. Rosenwasser ◽

B. T. Huber

Keyword(s):

Immune Response ◽

T Cell ◽

T Cell Activation ◽

Gene Function ◽

Cell Activation ◽

Immune Response Gene ◽

Response Gene

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B lymphocyte immune response gene phenotype is genetically determined.

Journal of Experimental Medicine ◽

10.1084/jem.155.4.1239 ◽

1982 ◽

Vol 155 (4) ◽

pp. 1239-1244

Author(s):

H Y Tse ◽

J J Mond ◽

D L Longo

Keyword(s):

Immune Response ◽

T Cells ◽

B Cells ◽

B Cell ◽

Gene Function ◽

B Lymphocyte ◽

Immune Response Gene ◽

Cell Immune Response ◽

Response Gene ◽

Genetically Determined

We examined the effects of the developmental milieu on the capacity of B cells to undergo immune response gene-controlled, T cell-dependent polyclonal proliferation. Although I-Aq poly(Glu60 Ala30 Tyr10)n (GAT)-nonresponder T cells developing in a responder environment become phenotypic GAT-responders, I-Aq B cells remain unresponsive to GAT, even after maturation in a GAT-responder animal. Conversely, (B10.A x B10.Q)F1 ([GAT responder x GAT nonresponder]F1) T cells developing in a B10.Q GAT nonresponder host fail to respond to GAT, but F1 B cells from the same F1 leads to parent chimeras make excellent proliferative responses in the presence of GAT and responder T cells. Thus, by this assay, B cell immune response gene function is genetically determined and is not affected by the developmental milieu.

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