Activated human T cells express a ligand for the human B cell‐associated antigen CD40 which participates in T cell‐dependent activation of B lymphocytes

Lane, Peter J. L.; Traunecker, André; Hubele, Sabine; Inui, Shigeru; Lanzavecchia, Antonio; Gray, David

doi:10.1002/eji.1830221016

Cited by 303 publications

(218 citation statements)

References 31 publications

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“…Recently Shoker et al (32) demonstrated heightened CD154 gene expression in CD4+ T-lymphocytes during acute and chronic renal rejection, which correlated with the severity of rejection. In contrast to other reported results they demonstrated constitutive CD154 gene expression in PBMCs (12,(33)(34)(35)(36)(37).…”

Section: Discussioncontrasting

confidence: 99%

Analysis of Intragraft Gene and Protein Expression of the Costimulatory Molecules, CD80, CD86 and CD154, in Orthotopic Liver Transplant Recipients

Bartlett¹,

McCall²,

Ameratunga³

et al. 2003

American Journal of Transplantation

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CD40-CD154 and/or CD28-CD80/86 costimulatory blockade induces long-term allograft survival in numerous animal models. Studies examining the expression of costimulatory molecules during acute cellular rejection (ACR) have been limited to renal and cardiac allografts.The aim of this study was to describe the relationship between intragraft costimulatory molecule expression in OLT recipients and ACR. Forty-five liver biopsies were obtained at reperfusion and day 7. Gene and protein expression of CD80, CD86 and CD154 were analyzed by RT-PCR and immunohistochemistry. CD154 protein expression was present in 13 of 18 patients with a RAI score of 4, but in only two of 14 patients with a RAI score of <4. There was a strong association between the RAI score and the presence of CD80 and CD154 immunoreactivity. CD86 protein expression did not correlate with the severity of ACR. In reperfusion biopsies CD154, but not CD80 or CD86, protein expression correlated with the total ischaemic time. There was no association between expression of costimulatory molecule genes and ACR.In conclusion, we have demonstrated an association between CD154 and CD80 protein expression and ACR in orthotopic liver allografts.

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Section: Discussioncontrasting

confidence: 99%

Analysis of Intragraft Gene and Protein Expression of the Costimulatory Molecules, CD80, CD86 and CD154, in Orthotopic Liver Transplant Recipients

Bartlett¹,

McCall²,

Ameratunga³

et al. 2003

American Journal of Transplantation

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“…These mechanisms probably serve to focus productive cognate contact-dependent CD40L+, CD4+ T cell interactions with appropriate target cells. However, CD40L expression may not be limited to CD4+ T cells since studies indicate that CD8+ T cells (41,44), mast cells (49, eosinophils (46), and B cells (47) also can express CD40L. Moreover, there is increased CD40L expression on peripheral blood CD4+ T cells, CD8+ T cells, and B cells in active SLE (48).…”

Section: Discussionmentioning

confidence: 99%

Immunohistologic analysis of renal CD40 and CD40L expression in lupus nephritis and other glomerulonephritides

Yellin

D’Agati

Parkinson

et al. 1997

Arthritis & Rheumatism

145

115

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Objective. To investigate potential mechanisms by which CD40L-mediated signals may be involved in the pathogenesis of lupus glomerulonephritis (GN).Methods. Renal in situ CD40L and CD40 expression was examined in patient biopsy specimens. Immunohistochemical studies were performed on frozen sections utilizing anti-CD40L monoclonal antibody (MAb), anti-CD40 MAb, or control MAb. As controls, we analyzed normal kidney specimens and specimens obtained from patients with IgA nephropathy, focal segmental glomerulosclerosis, minimal change disease, idiopathic membranous GN, and antineutrophil cytoplasmic antibodypositive pauci-immune GN. Staining distribution was noted and staining intensity scored on a semiquantitative scale of 0 (no staining) to 3+ (intense staining).Results. In normal kidney, CD40 was expressed on parietal epithelial cells, mesangial cells, endothelial cells, and distal tubules but not proximal tubules. Glomerular and tubular CD40 expression was markedly up-regulated in class I11 and class IV lupus GN, where there was intense staining of crescents, proximal and distal tubules, and interstitial mononuclear cells. In contrast, CD40 expression in class V lupus GN was similar to that in normal kidney. Interstitial mononuclear cells expressing CD40L were present in class IV lupus GN. However, these findings were not unique to lupus GN: up-regulation of CD40 and CD40L expres- Submitted for publication June 3, 1996; accepted in revised form July 17, 1996. sion was similarly observed in other inflammatory renal diseases.Conclusion. This study shows that CD40 is expressed on a variety of renal parenchymal and nonparenchymal cells in normal kidney. Renal CD40 expression is up-regulated in class I11 and class IV lupus nephritis, as well as in other inflammatory renal diseases, and is associated with the presence of CD40L+ mononuclear cells.

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“…T cell activation results in upregulation of CD40L expression [108][109][110], as well as upregulation of FasL expression [8], . As much as engagement of (constitutively expressed) B cell CD40 is necessary for T-dependent stimulation, CD40 triggering also upregulates Fas expression, and engagement of B cell Fas by T cell FasL initiates apoptotic events.…”

Section: Speculative Role For Fas-resistancementioning

confidence: 99%

Inducible resistance to Fas-mediated apoptosis in B cells

Rothstein

2000

Cell Res

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Apoptosis produced in B cells through Fas (APO-1, CD95) triggering is regulated by signals derived from other surface receptors: CD40 engagement produces upregulation of Fas expression and marked susceptibility to Fas-induced cell death, whereas antigen receptor engagement, or IL-4R engagement, inhibits Fas killing and in so doing induces a state of Fas-resistance, even in otherwise sensitive, CD40-stimulated targets. Surface immunoglobulin and IL-4R utilize at least partially distinct pathways to produce Fas-resistance that differentially depend on PKC and STAT6, respectively. Further, surface immunoglobulin signaling for inducible Fas-resistance bypasses Btk, requires NF-κB, and entails new macromolecular synthesis. Terminal effectors of B cell Fas-resistance include the known anti-apoptotic gene products, Bcl-xL and FLIP, and a novel anti-apoptotic gene that encodes FAIM (Fas Apoptosis Inhibitory Molecule). faim was identified by differential display and exists in two alter-

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Activated human T cells express a ligand for the human B cell‐associated antigen CD40 which participates in T cell‐dependent activation of B lymphocytes

Cited by 303 publications

References 31 publications

Analysis of Intragraft Gene and Protein Expression of the Costimulatory Molecules, CD80, CD86 and CD154, in Orthotopic Liver Transplant Recipients

Analysis of Intragraft Gene and Protein Expression of the Costimulatory Molecules, CD80, CD86 and CD154, in Orthotopic Liver Transplant Recipients

Immunohistologic analysis of renal CD40 and CD40L expression in lupus nephritis and other glomerulonephritides

Inducible resistance to Fas-mediated apoptosis in B cells

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