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author:("cafads, John")
1.  Intravenous Immunoglobulin as Salvage Therapy in Refractory Pyoderma Gangrenosum: Report of a Case and Review of the Literature 
Case Reports in Dermatology  2014;6(3):239-244.
Pyoderma gangrenosum is a neutrophilic dermatosis that occurs both as a primary disorder as well as secondary to an underlying disease. Due to its low prevalence there are limited data on therapeutics, particularly in refractory cases. Here, we discuss a case successfully managed with intravenous immunoglobulin and review the supporting literature.
doi:10.1159/000368824
PMCID: PMC4255992  PMID: 25493078
Intravenous immunoglobulin; Treatment; Pyoderma gangrenosum
3.  Expression Profile of FcγRIIb on Leukocytes and Its Dysregulation in Systemic Lupus Erythematosus1 
FcγRIIb (CD32B, Online Mendelian Inheritance in Man 604590), an IgG FcR with a tyrosine-based inhibitory motif, plays a critical role in the balance of tolerance and autoimmunity in murine models. However, the high degree of homology between FcγRIIb and FcγRIIa in humans and the lack of specific Abs to differentiate them have hampered study of the normal expression profile of FcγRIIb and its potential dysregulation in autoimmune diseases such as systemic lupus erythematosus (SLE). Using our newly developed anti-FcγRIIb mAb 4F5 which does not react with FcγRIIa, we found that FcγRIIb is expressed on the cell surface of circulating B lymphocytes, monocytes, neutrophils, myeloid dendritic cells (DCs), and at very low levels on plasmacytoid DCs from some donors. Normal donors with the less frequent 2B.4 promoter haplotype have higher FcγRIIb expression on monocytes, neutrophils, and myeloid DCs similar to that reported for B lymphocytes, indicating that FcγRIIb expression on both myeloid and lymphoid cells is regulated by the naturally occurring regulatory single nucleotide polymorphisms in the FCGR2B promoter. FcγRIIb expression in normal controls is up-regulated on memory B lymphocytes compared with naive B lymphocytes. In contrast, in active SLE, FcγRIIb is significantly down-regulated on both memory and plasma B lymphocytes compared with naive and memory/plasma B lymphocytes from normals. Similar down-regulation of FcγRIIb on myeloid-lineage cells in SLE was not seen. Our studies demonstrate the constitutive regulation of FcγRIIb by natural gene polymorphisms and the acquired dysregulation in SLE autoimmunity, which may identify opportunities for using this receptor as a therapeutic target.
PMCID: PMC2824439  PMID: 17312177

Results 1-3 (3)