Characterization of polymorphic forms of Fc receptor III on human neutrophils.

Ory, P A; Goldstein, Ira M.; Kwoh, Ely; Clarkson, S B

doi:10.1172/jci114067

Cited by 101 publications

(69 citation statements)

References 24 publications

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“…In addition to 29 kDa protein, human monocytes also express CD16 as a 50 -80-kDa protein (31,32). Human neutrophils show Fc␥RIII as 29, 33 kDa and a broad band at 50 to 73 kDa (33). In polymorphonuclear cells, 3G8 recognized broad bands at 64 -80 kDa, 50 -64 kDa and in natural killer cells at 53-59 kDa and 59 -65 kDa (34).…”

Section: T-cells Direct Staining With Monoclonal Anti-fc␥riii Antibomentioning

confidence: 99%

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Induced Expression of FcγRIIIa (CD16a) on CD4+ T Cells Triggers Generation of IFN-γhigh Subset

Chauhan

Chen

Moore

et al. 2015

Journal of Biological Chemistry

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Section: T-cells Direct Staining With Monoclonal Anti-fc␥riii Antibomentioning

confidence: 99%

“…IPs prepared using anti-CD16 (3G8) antibody after reducing and alkylating with iodoacetamide, revealed several bands from 20 to 37 kDa (33,35). In addition, a prominent band at ϳ 53 kDa was observed (Fig.…”

Section: T-cells Direct Staining With Monoclonal Anti-fc␥riii Antibomentioning

confidence: 99%

Induced Expression of FcγRIIIa (CD16a) on CD4+ T Cells Triggers Generation of IFN-γhigh Subset

Chauhan

Chen

Moore

et al. 2015

Journal of Biological Chemistry

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“…83,84 These two alleles differ in amino acid sequence and two glycosylation sites. 83,[85][86][87] Individuals who exhibit the Fc␥RIIIB-NA2/NA2 genotype have a decreased capacity to mediate phagocytosis than individuals with the Fc␥RIIIB-NA1/NA1 genotype. 88 Two studies have identified patients who express a rare NA-null allele, leading to a complete absence of the Fc␥RIIIB gene itself.…”

Section: Fc␥ Receptorsmentioning

confidence: 99%

The genetics of systemic lupus erythematosus: putting the pieces together

2002

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“…The spectrum of antigens implicated in antibody responses in autoimmune neutropenia include NA1, NA2, CD11a and CD11b, CD16, thyrotropin receptor-like molecules and membrane actin-like molecules [31,[34][35][36][37][38][39]. Due to the nature of serological assays, the specificity of the autoantibodies can be more or less precisely established.…”

Section: Discussionmentioning

confidence: 99%

Clonal predominance of CD8+ T cells in patients with unexplained neutropenia

Wlodarski

Nearman

Jiang

et al. 2008

Experimental Hematology

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Objective-T-cell-mediated autoimmunity may be involved in some cases of idiopathic neutropenia. We hypothesized that a precise T-cell receptor repertoire analysis may uncover cytotoxic T-cell (CTL) expansions that are less pronounced than those seen in T large granular lymphocyte leukemia (T-LGL), but are pathophysiologically analogous and thus can serve as markers of a T-cell-mediated process. Materials and Methods-Using rational algorithms for T-cell receptor analysis and in vivotracking of CTL responses previously established in our laboratory, we studied patients with unexplained chronic neutropenia (n = 20), T-LGL (n = 15), and healthy controls (n = 12). We further investigated the involvement of soluble inhibitory factors by coculture assays. To determine the level of immune activation, we studied interferon-g expression in CD8 + cells using Taqman polymerase chain reaction.Results-Fifteen expanded (immunodominant) CTL clones were detected in 12 of 20 patients. In comparison to LGL leukemia, these clones were less immunodominant, but clearly discernible from subclinical lymphoproliferations in controls. As a surrogate of cytotoxic activity, we found markedly increased production of interferon-γ in most of the neutropenia patients, irrespective of the presence of immunodominant CTL clones.Conclusions-These results suggest that, while immunodominant CTL clones are detectable in a proportion of patients only, CTL-mediated pathophysiology may be a general mechanism operating in idiopathic neutropenia. Oligogoclonal CTL expansions in chronic neutropenia may indicate an ongoing autoimmune process, while highly polarized monoclonalities in a subset of neutropenic LGL patients may represent the "extreme" end of the clonal continuum.Drugs, hereditary factors, infections, and intrinsic bone marrow diseases explain the etiology of most neutropenias. The inability to detect an immune-mediated process or other obvious cause often leads to diagnosis of chronic idiopathic neutropenia (CIN) [1][2][3][4][5][6]. Similarly, secondary autoimmune neutropenia (AIN), usually associated with collagen vascular diseases, lymphoproliferative disorders and viruses, is typically diagnosed by exclusion and thus relies on the quality of clinical and laboratory workups [6][7][8][9]. Lineage-restricted cytopenias, including neutropenia, have been associated with T-cell large granular lymphocyte leukemia It is likely that patients with AIN/CIN may belong to a heterogeneous group of diseases combining various autoimmune etiologies. Appearance of the bone marrow may reveal some clues as to the cellular targets of the autoimmune process; left shift could indicate that more mature cells are targets, while pure white cell aplasia suggests that very early myeloid precursors are affected. The similar target spectrum in AIN/CIN and T-LGL suggests that cytotoxic T-cell (CTL)-mediated autoimmunity can also operate in AIN/CIN. Consequently, detection of highly polarized CTL expansions in some cases of neutropenia patients may be consistent wi...

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Characterization of polymorphic forms of Fc receptor III on human neutrophils.

Abstract: We characterized Fc receptor III (FcR III) on human neutrophils and found it to be heavily glycosylated and polymorphic. In some individuals, FcR III that had been digested with Nglycanase appeared after SDS-PAGE under

Cited by 101 publications

References 24 publications

Induced Expression of FcγRIIIa (CD16a) on CD4+ T Cells Triggers Generation of IFN-γhigh Subset

Induced Expression of FcγRIIIa (CD16a) on CD4+ T Cells Triggers Generation of IFN-γhigh Subset

The genetics of systemic lupus erythematosus: putting the pieces together

Clonal predominance of CD8+ T cells in patients with unexplained neutropenia

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