Analysis of neonatally induced tolerance of H-2 alloantigens. III. Ease of abolition of tolerance of class I, but not class II, antigens with infusions of syngeneic, immunocompetent cells

R. S. Gruchalla, P. G. Strome, J. W. Streilein

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Neonatally-induced tolerance of class I H-2 alloantigens can be abolished in adult, long-term-tolerant mice by infusions of immunocompetent cells from donors syngeneic with the recipient. By contrast, neonatally-induced tolerance of Ia alloantigens can not be abolished easily, indicating that the Ia-specific tolerant state is maintained by an active process that can be impressed upon mature alloreactive lymphoid cells in the tolerant environment. This finding is concordant with previous observations that tolerance of Ia alloantigens can readily be transferred adoptively by inoculating lymphoid cells from tolerant mice into syngeneic, naive recipients. It is concluded that class II H-2 antigens induce a type of unresponsiveness that class I antigens fail to evoke, an unresponsiveness that is actively maintained among mature immunocompetent cells. It is proposed that, in addition to a central process of clonal deletion/inactivation that both class I and class II H-2 antigens induce in neonatal mice, Ia alloantigens also evoke a secondary, fail-safe mechanism that operates to prevent alloreactivity from emerging when cells with alloreactive potential escape the central mechanism, or mutate to alloreactivity at a later stage of maturation.

Original languageEnglish (US)
Pages (from-to)318-323
Number of pages6
JournalTransplantation
Volume36
Issue number3
StatePublished - 1983

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Isoantigens
Histocompatibility Antigens Class II
H-2 Antigens
Clonal Deletion
Lymphocytes
Histocompatibility Antigens Class I

ASJC Scopus subject areas

  • Immunology
  • Transplantation

Cite this

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title = "Analysis of neonatally induced tolerance of H-2 alloantigens. III. Ease of abolition of tolerance of class I, but not class II, antigens with infusions of syngeneic, immunocompetent cells",
abstract = "Neonatally-induced tolerance of class I H-2 alloantigens can be abolished in adult, long-term-tolerant mice by infusions of immunocompetent cells from donors syngeneic with the recipient. By contrast, neonatally-induced tolerance of Ia alloantigens can not be abolished easily, indicating that the Ia-specific tolerant state is maintained by an active process that can be impressed upon mature alloreactive lymphoid cells in the tolerant environment. This finding is concordant with previous observations that tolerance of Ia alloantigens can readily be transferred adoptively by inoculating lymphoid cells from tolerant mice into syngeneic, naive recipients. It is concluded that class II H-2 antigens induce a type of unresponsiveness that class I antigens fail to evoke, an unresponsiveness that is actively maintained among mature immunocompetent cells. It is proposed that, in addition to a central process of clonal deletion/inactivation that both class I and class II H-2 antigens induce in neonatal mice, Ia alloantigens also evoke a secondary, fail-safe mechanism that operates to prevent alloreactivity from emerging when cells with alloreactive potential escape the central mechanism, or mutate to alloreactivity at a later stage of maturation.",
author = "Gruchalla, {R. S.} and Strome, {P. G.} and Streilein, {J. W.}",
year = "1983",
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pages = "318--323",
journal = "Transplantation",
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T1 - Analysis of neonatally induced tolerance of H-2 alloantigens. III. Ease of abolition of tolerance of class I, but not class II, antigens with infusions of syngeneic, immunocompetent cells

AU - Gruchalla, R. S.

AU - Strome, P. G.

AU - Streilein, J. W.

PY - 1983

Y1 - 1983

N2 - Neonatally-induced tolerance of class I H-2 alloantigens can be abolished in adult, long-term-tolerant mice by infusions of immunocompetent cells from donors syngeneic with the recipient. By contrast, neonatally-induced tolerance of Ia alloantigens can not be abolished easily, indicating that the Ia-specific tolerant state is maintained by an active process that can be impressed upon mature alloreactive lymphoid cells in the tolerant environment. This finding is concordant with previous observations that tolerance of Ia alloantigens can readily be transferred adoptively by inoculating lymphoid cells from tolerant mice into syngeneic, naive recipients. It is concluded that class II H-2 antigens induce a type of unresponsiveness that class I antigens fail to evoke, an unresponsiveness that is actively maintained among mature immunocompetent cells. It is proposed that, in addition to a central process of clonal deletion/inactivation that both class I and class II H-2 antigens induce in neonatal mice, Ia alloantigens also evoke a secondary, fail-safe mechanism that operates to prevent alloreactivity from emerging when cells with alloreactive potential escape the central mechanism, or mutate to alloreactivity at a later stage of maturation.

AB - Neonatally-induced tolerance of class I H-2 alloantigens can be abolished in adult, long-term-tolerant mice by infusions of immunocompetent cells from donors syngeneic with the recipient. By contrast, neonatally-induced tolerance of Ia alloantigens can not be abolished easily, indicating that the Ia-specific tolerant state is maintained by an active process that can be impressed upon mature alloreactive lymphoid cells in the tolerant environment. This finding is concordant with previous observations that tolerance of Ia alloantigens can readily be transferred adoptively by inoculating lymphoid cells from tolerant mice into syngeneic, naive recipients. It is concluded that class II H-2 antigens induce a type of unresponsiveness that class I antigens fail to evoke, an unresponsiveness that is actively maintained among mature immunocompetent cells. It is proposed that, in addition to a central process of clonal deletion/inactivation that both class I and class II H-2 antigens induce in neonatal mice, Ia alloantigens also evoke a secondary, fail-safe mechanism that operates to prevent alloreactivity from emerging when cells with alloreactive potential escape the central mechanism, or mutate to alloreactivity at a later stage of maturation.

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