T helper cell‐dependent induction of resting B cell differentiation need not require cognate cell interactions

Julius, Michael; Rammensee, Hans‐Georg

doi:10.1002/eji.1830180309

Cited by 26 publications

(6 citation statements)

References 28 publications

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“…In any case, the fact that there was suppression does not affect the interpretation of a preference for direct T-B interactions for three reasons: (a) The recovery of the suppressed allotype of IgG2a in eight strongly suppressed mice did not result in antichromatin autoantibodies of that allotype ; (b) the presence of the noncognate allotype in 5 mice that were only partially suppressed for IgG2a did not result in antichromatin autoantibodies of that allotype ; (c) the IgM antichromatin antibodies were principally of the cognate allotype. Our current work on autoimmunity parallels results with exogenous antigens (9,10,(33)(34)(35)(36)(37)(38)(39)(40) . In an in vivo model cognate T-B collaboration was clearly preferred (38).…”

Section: Discussionsupporting

confidence: 69%

Autoantibodies in chronic graft versus host result from cognate T-B interactions.

Morris

Cheek

Cohen

et al. 1990

The Journal of Experimental Medicine

126

111

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A chronic graft-versus-host reaction (GVH) induced in nonautoimmune mice causes a syndrome that closely resembles SLE. In this model, donor T cells react against incompatible host Ia structures and generate excessive help, which activates a subpopulation of self-reactive B cells. We have studied whether these self-reactive B cells are activated by direct interaction with alloreactive T cells or by nonspecific bystander effects. Two types of chimeras were made: double-parental chimeras, differing at both Ia and Igh allotype [B6.C20 + bm12----(B6.C20 x bm12)F1]; and control chimeras [(B6.C20 x bm12)F1----(B6.C20 x bm12)F1]. A chronic GVH syndrome was induced in the chimeras by infusion of B6 or bm12 spleen cells. Coombs and antichromatin autoantibodies were measured using Igh allotype-specific immunoassays. The double-parental chimeras that received bm12 cells made autoantibodies principally of the Igha allotype, indicating that the bm12 T cells interacted only with the Iab-bearing host B cells. Conversely, double-parental chimeras that received B6 cells made mostly Ighb autoantibodies, indicating direct cognate interaction with the Iabm12-bearing host B cells. The control chimeras made autoantibodies of both allotypes. These results indicate that autoantibodies in chronic GVH result from direct T-B interactions and not from nonspecific T cell-derived factors.

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Section: Discussionsupporting

confidence: 69%

Autoantibodies in chronic graft versus host result from cognate T-B interactions.

Morris

Cheek

Cohen

et al. 1990

The Journal of Experimental Medicine

126

111

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“…It is known that ab T cells can induce polyclonal proliferation of naive B cells when the cells are ligated via mitogens or anti-TcR antibodies [35,36]. gd T cells may also activate B cells, at least under certain in vivo conditions and notably in the absence of ab T cells [37,38].…”

Section: Ability Of Dn2b4a þ T Cells To Induce B-cell Proliferationmentioning

confidence: 99%

γδ T‐Cell Precursor‐Derived CD4⁻ CD8⁻αβ T Cells Retain γδ Cell Function

Fritsch

Ivars

1998

Scand J Immunol

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Fritsch M, Ivars F. gd T-Cell Precursor-Derived CD4 -CD8 -ab T Cells Retain gd Cell Function. Scand J Immunol 1998;48:8-14 We have previously shown that some of the DNab þ T cells arising in TcRa-chain transgenic mice are of gd T cell origin, based on phenotypic data and on their status of TcR gene rearrangements. In the present report we investigated the impact of ab TcR expression on the functional programme of the mature gd precursorderived DNab þ T cells. Our results demonstrate that both their proliferative capacity and their cytokine production profile are similar to that of gd T cells. Furthermore, both transgenic DNab þ T cells and DNgd þ T cells up-regulate CD8a expression after activation, but, in contrast to CD4 þ ab T cells, are unable to induce proliferation of naive B cells. Thus, our results suggest that the effector functions of mature T cells are determined independently of the TcR isotype, probably at an early stage of differentiation, and thereby have important implications for current models of T-cell lineage commitment.

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“…Although the inductive phase of T cell help is Ag depen-dent and MHC restricted (5, 10-15, 34, 35), the effector phase of Th function can be Ag independent and MHC nonrestricted (25,28,30,34,(36)(37)(38)(39)(40)(41)(42)(43). An additional contrasting feature is that the inductive phase of T cell help often requires CD4 molecules and is inhibited by anti-CD4 mAb (16), whereas helper effector function does not require CD4 molecules (44) and is not inhibited by anti-CD4 mAbs (27,28,30,42).…”

mentioning

confidence: 99%

Identification of a novel surface protein on activated CD4+ T cells that induces contact-dependent B cell differentiation (help).

Lederman

Yellin

Krichevsky

et al. 1992

The Journal of Experimental Medicine

330

192

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SummaryCD4 + T lymphocytes provide contact-dependent stimuli to B cells that are critical for the generation of specific antibody responses in a process termed T helper function. The surface structures on activated CD4 + T cells that mediate this function are not fully known. We previously reported the isolation of a functionally unique subclone of the Jurkat leukemic T cell line (D1.1) that constitutively expressed contact-dependent helper effector function. To identify T cell surface molecules that mediate contact-dependent T helper function, a monoclonal antibody (mAb), designated 5c8, was generated that inhibits Dl.l-mediated B cell activation and immunoprecipitates a novel 30-kD protein structure from surface-iodinated D1.1 cells. Normal CD4 + T cells express 5c8 antigen (Ag) transiently after activation by phorbol myristate acetate and phytohemagglutinin with maximal expression 5-6 h after activation and absence of expression by 24 h. In contrast, neither resting nor activated CD8 § T cells express 5c8 Ag. In functional studies, mAb 5c8 inhibits the ability of fixed, activated CD4 § T cells to induce B cell surface CD23 expression. In addition, mAb 5c8 inhibits the ability of CD4 + T cells to direct terminal B cell differentiation driven by pokeweed mitogen. Taken together, these data suggest that 5c8 Ag is a novel, activation-induced surface T cell protein that is involved in mediating a contactdependent element of the helper effector function of CD4 § T lymphocytes.I n a contact-dependent process, termed T helper (Th) function, CD4 + T lymphocytes direct the activation and differentiation of B lymphocytes and thereby regulate the humoral immune response by modulating the specificity, secretion and isotype-encoded effector functions of antibody molecules (1-7). The T cell surface molecules that mediate the contact-dependent elements of Th cell function are not fully known.The process by which T cells help B cells to differentiate has been divided into two distinct phases: the inductive and the effector (8, 9). In the inductive phase, resting T cells contact antigen-primed B cells and this association allows clonotypic TCR-CD4 complexes to interact with Ia/Ag complexes on B cells (5, 10-16). TCP,/CD4 recognition of Ia/Ag results in the formation of stable T-B cognate pairs and bidirectional T and B cell activation (17-22). In the effector phase, activated T cells drive B cell differentiation by secreting lymphokines (23, 24) and by contact-dependent stimuli (20,(25)(26)(27)(28)(29)(30)(31)(32), both of which are required for T cells to drive small, resting B cells to terminally differentiate into Ig-secreting cells (25, 33, 34).Although the inductive phase of T cell help is Ag dependent and MHC restricted (5, 10-15, 34, 35), the effector phase of Th function can be Ag independent and MHC nonrestricted (25, 28, 30, 34,(36)(37)(38)(39)(40)(41)(42)(43)). An additional contrasting feature is that the inductive phase of T cell help often requires CD4 molecules and is inhibited by anti-CD4 mAb (16), whereas help...

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T helper cell‐dependent induction of resting B cell differentiation need not require cognate cell interactions

Cited by 26 publications

References 28 publications

Autoantibodies in chronic graft versus host result from cognate T-B interactions.

Autoantibodies in chronic graft versus host result from cognate T-B interactions.

γδ T‐Cell Precursor‐Derived CD4⁻ CD8⁻αβ T Cells Retain γδ Cell Function

Identification of a novel surface protein on activated CD4+ T cells that induces contact-dependent B cell differentiation (help).

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T helper cell‐dependent induction of resting B cell differentiation need not require cognate cell interactions

Cited by 26 publications

References 28 publications

Autoantibodies in chronic graft versus host result from cognate T-B interactions.

Autoantibodies in chronic graft versus host result from cognate T-B interactions.

γδ T‐Cell Precursor‐Derived CD4− CD8−αβ T Cells Retain γδ Cell Function

Identification of a novel surface protein on activated CD4+ T cells that induces contact-dependent B cell differentiation (help).

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γδ T‐Cell Precursor‐Derived CD4⁻ CD8⁻αβ T Cells Retain γδ Cell Function