Authentic T helper CD4 (W3/25) antigen on rat peritoneal macrophages.

Jefferies, Wilfred A.; Green, Jon R.; Williams, Alan F.

doi:10.1084/jem.162.1.117

Cited by 311 publications

(102 citation statements)

References 24 publications

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“…HIS25 (CD45RC; LCA isotype present on all Tcyt/suppr., part of Th and all B cells) [46] and HIS51 (Thy1.1, within the TCR + cell population specific for RTE) [47] were produced by the Department of Histology, University of Groningen, The Netherlands. W3/25 (CD4) [48], OX6 (RT1B; MHC class II) [49], OX22 (CD45RC) [50] and OX35 (CD4) [14] were obtained from the European Collection of Animal Cell Culture (Salisbury, UK). PEconjugated OX8 (CD8 , Tcyt/suppr.…”

Section: Antibodiesmentioning

confidence: 99%

Susceptibility to clinically manifest cyclosporine A (CsA)-induced autoimmune disease is associated with interferon-gamma (IFN-γ)-producing CD45RC+RT6− T helper cells

Beijleveld

Groen

Broeren

et al. 1996

Clinical and Experimental Immunology

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SUMMARYLethally irradiated Lewis (LEW) rats reconstituted with syngeneic bone marrow and given CsA for a 4-week period, develop, upon withdrawal of CsA, a graft-versus-host-like disease, so-called CsA-induced autoimmunity (CsA-AI). This T cell-mediated autoimmune disease is thymus-dependent; it is generally held that this disease is a consequence of aberrant T cell recovery brought about by CsA. In this study we determined mononuclear cell subsets phenotypically by tri-colour flow cytometry. A strong decrease in recent thymic emigrants (Thy1.1 + , TCR ® ¯ + ) was observed as a consequence of CsA treatment, eventually resulting in decreased absolute peripheral T cell numbers. In these rats no altered CD4:CD8 T cell ratio was observed before onset of CsA-AI; CD4 + and CD8 + cells consisted predominantly of monocytes (CD4 dim+ , TCR ® ¯ -) and natural killer cells (CD8 + , TCR ® ¯ -), respectively. LEW rats, xirradiated, syngeneic bone marrow-reconstituted and treated with CsA, showed a marked and persistent, relative expansion of mature CD45RC + , RT6 -Th cells. In contrast, Brown-Norway rats treated in a similar fashion, or LEW rats subjected to either CsA treatment or x-irradiation, did not show a comparable expansion of mature CD45RC + , RT6 -Th cells, nor did these animals develop CsA-AI. The CD45RC + , RT6 -Th cells produced IL-2, and moreover constituted the only Th subset producing IFN-°u pon stimulation, and therefore were considered as Th1-like effector cells. These results are consistent with the view that a persistent preponderance of Th1 cells and not the mere presence of autoreactive cells determines whether or not clinically manifest CsA-AI will occur.

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Section: Antibodiesmentioning

confidence: 99%

Susceptibility to clinically manifest cyclosporine A (CsA)-induced autoimmune disease is associated with interferon-gamma (IFN-γ)-producing CD45RC+RT6− T helper cells

Beijleveld

Groen

Broeren

et al. 1996

Clinical and Experimental Immunology

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“…Cell surface expression of CD4 or CD8␣ was examined by (double) staining with FITC-conjugated anti-CD4 mAb (W3/25 or OX35, which bind to different domains of CD4 (domains 1 and 2, respectively) and do not compete for binding (30) or with FITC-conjugated anti-CD8␣ mAb and PEconjugated mouse anti-rat CD25 mAb. Activation-induced modulation of TCR␣␤ on CD4 ϩ cells was measured with FITC-conjugated anti-TCR␣␤ and PE-conjugated anti-CD4 mAb.…”

Section: Flow Cytometrymentioning

confidence: 99%

Glucocorticoids Regulate TCR-Induced Elevation of CD4: Functional Implications

Wiegers

Stec

Klinkert

et al. 2000

The Journal of Immunology

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CD4 serves as a coreceptor during Ag recognition by the TCR. This interaction results in a marked increase in the sensitivity of a T cell to Ag presented by MHC class II molecules. Here we report that activation of T cells either by plate-bound mAb (anti-TCR, anti-CD3) or soluble activators (staphylococcal enterotoxin A, Con A) is associated with an (up to 3-fold) increase in CD4 cell surface expression on CD25+ cells, which was maximal after 72–96 h. Incubation with the glucocorticoid hormone corticosterone (CORT) shifted the enhancement of CD4 expression to a point about 24 h earlier than that observed in control cultures. In parallel, the proliferative response of these CORT-treated cells was profoundly enhanced. An involvement of increased CD4 expression in this enhanced proliferative response was evidenced by the observation that T cell proliferation in CORT-treated cultures was much less sensitive to inhibition by an inhibitory, nondepleting anti-CD4 mAb than that in control cultures. TCR down-regulation was, however, not affected by CORT. Thus, based on this study and previous reports we propose that both TCR-mediated signals and glucocorticoids are important physiological regulators of CD4 expression. In addition, these findings may be of significance for the sensitivity of CD4+ cells to HIV infection upon T cell activation, as the efficacy of primary patient HIV entry depends on the level of surface CD4.

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“…Recipients were characterized for engraftment using flow cytometry (FACSort; Becton Dickinson, Mountain View, CA) to determine the percentage of PBL bearing H-2 b (B10), H-2 k (B10.BR), and H-2 d (B10.D2) surface Ags, as previously described (13). Briefly, peripheral blood was collected into heparinized plastic serum vials containing 200 l of Medium 199 and separated over 3 ml of lymphocyte separation medium (LSM; Organon Teknik, Durham, NC) at 37°C at 400 ϫ g for 25 min.…”

Section: Characterization Of Chimeras By Flow Cytometrymentioning

confidence: 99%

The Abrogation of Allosensitization Following the Induction of Mixed Allogeneic Chimerism

Colson

Schuchert²,

Ildstad

2000

The Journal of Immunology

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The association of preformed anti-donor Abs with the hyperacute rejection of bone marrow and solid organ allografts and the persistence of the anti-donor immune response secondary to immunologic memory make allosensitization an absolute contraindication to transplantation. Mixed allogeneic (A + B→A) bone marrow chimerism has been demonstrated to confer donor-specific tolerance in nonsensitized recipients, but has not been evaluated in the setting of allosensitization. The current study documents that despite significant anti-donor sensitization, mixed allogeneic engraftment is possible and provides a marked advantage over fully allogeneic (B→A) models. Moreover, the acceptance of donor skin grafts and loss of circulating anti-donor Abs suggest that allosensitization can be abrogated with the induction of stable mixed allogeneic chimerism.

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Authentic T helper CD4 (W3/25) antigen on rat peritoneal macrophages.

Cited by 311 publications

References 24 publications

Susceptibility to clinically manifest cyclosporine A (CsA)-induced autoimmune disease is associated with interferon-gamma (IFN-γ)-producing CD45RC+RT6− T helper cells

Susceptibility to clinically manifest cyclosporine A (CsA)-induced autoimmune disease is associated with interferon-gamma (IFN-γ)-producing CD45RC+RT6− T helper cells

Glucocorticoids Regulate TCR-Induced Elevation of CD4: Functional Implications

The Abrogation of Allosensitization Following the Induction of Mixed Allogeneic Chimerism

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