A clonal deletion model for Ir gene control of the immune response.
about
Helper T-cell clones that recognize autologous insulin are stimulated in nonresponder mice by pork insulinGene 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 cellAdaptive differentiation of murine lymphocytes. IV (Responder x nonresponder) F1 T cells can be taught to preferentially help nonresponder, rather than responder, B cellsAntigen-specific T cell clones restricted to unique F1 major histocompatibility complex determinants. Inhibition of proliferation with monoclonal anti-Ia antibodyAntigen-reactive T clones. III. Low responder antigen-presenting cells function effectively to present antigen to selected T cell clones derived from (High Responder x Low Responder)F1 mice.Murine syngeneic mixed lymphocyte response. I. Target antigens are self Ia moleculesGeneration of T cell colonies from responder strain 2 guinea pigs that recognize the copolymer L-glutamic acid, L-lysine in association with nonresponder strain 13 Ia antigens.Restriction molecules involved in the interaction of T cells with allogeneic antigen-presenting cellsIn vitro correlate for a clonal deletion mechanism of immune response gene-controlled nonresponsiveness.Neonatal tolerance of major histocompatibility complex antigens alters Ir gene control of the cytotoxic T cell response to vaccinia virus.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 reSelective modification of a private I-A allo-stimulating determinant(s) upon association of antigen with an antigen-presenting cellDistinct recognition phenotypes exist for T cell clones specific for small peptide regions of proteins. Implications for the mechanisms underlying major histocompatibility complex-restricted antigen recognition and clonal deletion models of immune rThe cytotoxic T cell response to the male-specific histocompatibility antigen (H-Y) is controlled by two dominant immune response genes, one in the MHC, the other in the Tar alpha-locusPossible mechanisms by which the H-2Kbm3 mutation may decrease cytotoxic T-lymphocyte recognition of vesicular stomatitis virus nucleoprotein antigen.Distinct H-2-linked Ir genes control both antibody and T cell responses to different determinants on the same antigen, myoglobin.Nonresponsiveness to an immunodominant Epstein-Barr virus-encoded cytotoxic T-lymphocyte epitope in nuclear antigen 3A: implications for vaccine strategiesThe role of H-2 linked genes in helper T-cell function. IV. Importance of T-cell genotype and host environment in I-region and Ir gene expression.Significance and biological function of class II MHC molecules. Rous-Whipple Award lecture 1985.The influence of MHC gene products on the generation of an antigen-specific T-cell repertoire.
P2860
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P2860
A clonal deletion model for Ir gene control of the immune response.
description
1978 nî lūn-bûn
@nan
1978年の論文
@ja
1978年学术文章
@wuu
1978年学术文章
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1978年学术文章
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1978年学术文章
@zh-my
1978年学术文章
@zh-sg
1978年學術文章
@yue
1978年學術文章
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1978年學術文章
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name
A clonal deletion model for Ir gene control of the immune response.
@en
A clonal deletion model for Ir gene control of the immune response.
@nl
type
label
A clonal deletion model for Ir gene control of the immune response.
@en
A clonal deletion model for Ir gene control of the immune response.
@nl
prefLabel
A clonal deletion model for Ir gene control of the immune response.
@en
A clonal deletion model for Ir gene control of the immune response.
@nl
P2860
P1476
A clonal deletion model for Ir gene control of the immune response.
@en
P2093
Schwartz RH
P2860
P356
10.1111/J.1365-3083.1978.TB00420.X
P577
1978-01-01T00:00:00Z