T cell differentiation and generation of the antigen-specific T cell repertoire in man: observations in MHC class II deficiency

Mannhalter, Josef W.; Wolf, Hermann M.; Hauber, Ilona; Miricka, M.; Gadner, Helmut; Eibl, Martha M.

doi:10.1111/j.1365-2249.1994.tb06100.x

Cited by 5 publications

(1 citation statement)

References 27 publications

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“…Blocking SupT1-CIITA B5 cells with an HLA-DP-specific monoclonal or a pan-reactive MHC class II Ab did not return the level of HIV infection of CIITA-expressing cells to that of SupT1 cells ( by CD4 not only induces the conformational change required to expose gp41 (fusion peptide) but may allow for an interaction with a CIITA-regulated, T cell-specific ligand that either stabilizes virus binding or promotes more efficient fusion. (50,51), suggesting that although these cells were MHC class II-negative, CIITA was still transcriptionally active. Our data confirm that cellular HLA-DR is not involved in CIITA-enhanced attachment of HIV virions to cells.…”

Section: Blocking Of Surface Hla-dp Does Not Reduce Enhanced Infectiomentioning

confidence: 99%

CIITA Enhances HIV-1 Attachment to CD4+ T Cells Leading to Enhanced Infection and Cell Depletion

Porter¹,

Kelley²,

Nekorchuk³

et al. 2010

The Journal of Immunology

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Activated CD4+ T cells are more susceptible to HIV infection than resting T cells; the reason for this remains unresolved. Induction of CIITA and subsequent expression of the MHC class II isotype HLA-DR are hallmarks of CD4+ T cell activation; therefore, we investigated the role of CIITA expression in T cells during HIV infection. CIITA-expressing SupT1 cells display enhanced virion attachment in a gp160/CD4-dependent manner, which results in increased HIV infection, virus release, and T cell depletion. Although increased attachment and infection of T cells correlated with HLA-DR surface expression, Ab blocking, transient expression of HLA-DR without CIITA, and short hairpin RNA knockdown demonstrate that HLA-DR does not directly enhance susceptibility of CIITA-expressing cells to HIV infection. Further analysis of the remaining MHC class II isotypes, HLA-DP and HLA-DQ, MHC class I isotypes, HLA-A, HLA-B, and HLA-C, and the class II Ag presentation genes, invariant chain and HLA-DM, demonstrate that these proteins likely do not contribute to CIITA enhancement of HIV infection. Finally, we demonstrate that in activated primary CD4+ T cells as HLA-DR/CIITA expression increases there is a corresponding increase in virion attachment. Overall, this work suggests that induction of CIITA expression upon CD4+ T cell activation contributes to enhanced attachment, infection, virus release, and cell death through an undefined CIITA transcription product that may serve as a new antiviral target.

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Section: Blocking Of Surface Hla-dp Does Not Reduce Enhanced Infectiomentioning

confidence: 99%

CIITA Enhances HIV-1 Attachment to CD4+ T Cells Leading to Enhanced Infection and Cell Depletion

Porter¹,

Kelley²,

Nekorchuk³

et al. 2010

The Journal of Immunology

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Biologic Consequences of Defective Major Histocompatibility Complex Class II Presentation

Eibl

Wolf

1998

Current Topics in Microbiology and Immunology

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Major Histocompatibility Complex Class II Deficiency Needs an Early Diagnosis: Report of a Case

Canioni

Patey

Cuenod

et al. 1997

Pediatric Pathology & Laboratory Medicine

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Major histocompatibility complex (MHC) class II deficiency is a rare primary immunodeficiency disorder characterized by defects in human leukocyte antigen class II expression, inconsistent expression of human leukocyte class I molecules, and a lack of cellular and humoral immune responses to foreign antigens. Clinical onset occurs early in life with recurrent infections and chronic diarrhea. The prognosis is poor, and mean age at the time of death is 4 years. The only curative treatment is bone marrow transplantation (BMT), which allows the immune system's reconstitution. BMT should be done early in life, because long-term survival seems to depend on the number of previous viral infections. We report the case of an MHC class II deficiency discovered late in a 4-year-old girl by means of immunohistochemistry of small bowel biopsy revealing the absence of MHC class II expression. The child received a BMT twice but died because of a overwhelming viral infection. This case underlines the necessity to explore children presenting with infections and chronic diarrhea in order to find MHC class II deficiency. Usually, diagnosis is performed on cytospins, but when it has been missed clinically, it can be performed by using immunohistochemistry on small bowel biopsies.

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T cell differentiation and generation of the antigen-specific T cell repertoire in man: observations in MHC class II deficiency

Cited by 5 publications

References 27 publications

CIITA Enhances HIV-1 Attachment to CD4+ T Cells Leading to Enhanced Infection and Cell Depletion

CIITA Enhances HIV-1 Attachment to CD4+ T Cells Leading to Enhanced Infection and Cell Depletion

Biologic Consequences of Defective Major Histocompatibility Complex Class II Presentation

Major Histocompatibility Complex Class II Deficiency Needs an Early Diagnosis: Report of a Case

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