Expression of major histocompatibility class II antigens on polymorphonuclear neutrophils in patients with Wegener's granulomatosis

Hänsch, Gertrud Maria; Radsak, Markus P.; Wagner, C.; Reis, Bettina; Koch, Armin; Breitbart, A; Andrássy, K.

doi:10.1046/j.1523-1755.1999.00446.x

Cited by 38 publications

(38 citation statements)

References 26 publications

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“…The present study confirms these data and provides evidence that PMN express constitutively IL-2R. (Haensch, et al, 1999). The close correlation of HLA class II expression to disease activity prompted the present study with the objective of investigating whether or not HLA class II-positive PMN might activate or support activation of T lymphocytes.…”

Section: Discussionsupporting

confidence: 86%

Human Leukocyte Antigen Class II in Stimulated Polymorphnuclear Neutrophils

Abdel-Salam¹

2012

Histocompatibility

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Section: Discussionsupporting

confidence: 86%

Human Leukocyte Antigen Class II in Stimulated Polymorphnuclear Neutrophils

Abdel-Salam¹

2012

Histocompatibility

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“…Expression by PMN of MHC class II and CD83, a phenomenon termed 'transdifferentiation' , can be also induced in vitro by cultivating the PMN with either IFN-γ or TNF-α, and also results in the ability of those PMN to present superantigens to T cells [12,[23][24][25][26][27]. Moreover, up-regulation of these antigens was also observed in chronic inflammatory disease [28][29][30]. At variance with these data, we could now show that persistent bacterial infection also induces the transdifferentiation of PMN.…”

Section: Discussionmentioning

confidence: 99%

Cellular inflammatory response to persistent localizedStaphylococcus aureusinfection: phenotypical and functional characterization of polymorphonuclear neutrophils (PMN)

Wagner

Iking‐Konert

Hug

et al. 2005

Clinical and Experimental Immunology

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SummaryPersistent, localized Staphylococcus aureus infections, refractory to antibiotic treatment, can result in massive tissue destruction and surgical intervention is often the only therapeutic option. In that context, we investigated patients with S. aureus -induced infection at various sites, apparent as either olecranon bursitis, empyema of the knee joint or soft tissue abscess formation. As expected, a prominent leucocyte infiltrate was found, consisting predominantly of polymorphonuclear neutrophils (PMN) (up to 75%) and to a lesser extent of T lymphocytes and natural killer (NK) cells. In line with their bactericidal capacity, PMN expressed the high-affinity receptor for IgG, CD64 and the lipopolysaccharide (LPS) receptor CD14; moreover, the oxygen radical production in response to the bacterial peptide f-MLP was enhanced, while chemotactic activity was greatly reduced. The more intriguing finding, however, was that a portion of PMN had acquired major histocompatibility complex (MHC) class II antigens and CD83, indicative of a transdifferentiation of PMN to cells with dendritic-like characteristics. Of note is that a similar transdifferentiation can be induced in PMN in vitro , e.g. by gamma interferon or by tumour necrosis factor alpha. Co-cultivation of transdifferentiated PMN with autologous T lymphocytes resulted in prominent T cell proliferation, provided that S. aureus enterotoxin A was added. Taken together, persistent S. aureus infection induces PMN to acquire characteristics of dendritic cells, which in turn might promote the local immune response.

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“…18 In disease, DRB1 family proteins can be detected on the cell surface induced by certain cytokines, 19 -22 including a report that MHC II surface expression is detected on neutrophils of patients with active Wegener's granulomatosis but not on neutrophils of patients with inactive disease. 19 We asked if surface-expressed DRB1*15 would bind sense-PR3 and/or complementary-PR3 peptides. Untreated neutrophils from patients, who were genotyped as DRB1*15,*15, were shown to have intracellular pools of MHC-DRB1 protein (Supplemental Figure 2A).…”

Section: -163mentioning

confidence: 99%

DRB1*15 Allele Is a Risk Factor for PR3-ANCA Disease in African Americans

Cao

Schmitz²,

Yang³

et al. 2011

Journal of the American Society of Nephrology

106

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Anti-neutrophil cytoplasmic autoantibody (ANCA) disease rarely occurs in African Americans and risk factors for the disease in this population are unknown. Here, we genotyped MHC class II alleles and found that, among African Americans, those with proteinase 3-ANCA (PR3-ANCA) had 73.3-fold higher odds of having HLA-DRB1*15 alleles than community-based controls (OR 73.3; 95% CI 9.1 to 591). In addition, a disproportionate number of African American patients carried the DRB1*1501 allelic variant of Caucasian descent rather than the DRB1*1503 allelic variant of African descent. Among Caucasians, those with PR3-ANCA had 2.2-fold higher odds of carrying DRB1*1501 than controls (OR 2.2; 95% CI 1.2 to 4.0). A validation study supported by the Vasculitis Clinical Research Consortium confirmed the strong association between the DRB1*15 allele and PR3-ANCA disease, among African Americans. Furthermore, we found that DRB1*1501 protein binds with high affinity to amino acid sequences of sense-PR3, purportedly an antigenic epitope, and to the amino acid sequence complementary to this epitope in vitro. Peptides of sense-PR3 and complementary-PR3 also bound to TNF-␣-induced surface expression of DRB1*1501 on peripheral neutrophils. Taken together, these data suggest HLA-DRB1*15 alleles contribute to the pathogenesis of PR3-ANCA disease.

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Expression of major histocompatibility class II antigens on polymorphonuclear neutrophils in patients with Wegener's granulomatosis

Cited by 38 publications

References 26 publications

Human Leukocyte Antigen Class II in Stimulated Polymorphnuclear Neutrophils

Human Leukocyte Antigen Class II in Stimulated Polymorphnuclear Neutrophils

Cellular inflammatory response to persistent localizedStaphylococcus aureusinfection: phenotypical and functional characterization of polymorphonuclear neutrophils (PMN)

DRB1*15 Allele Is a Risk Factor for PR3-ANCA Disease in African Americans

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