J 2012

B-lymphocyte Subpopulations in Patients with Selective IgA Deficiency

NECHVÁTALOVÁ, Jana; Zdenka PIKULOVÁ; Dagmar STIKAROVSKÁ; Sáva PEŠÁK; Marcela VLKOVÁ et al.

Základní údaje

Originální název

B-lymphocyte Subpopulations in Patients with Selective IgA Deficiency

Autoři

NECHVÁTALOVÁ, Jana; Zdenka PIKULOVÁ; Dagmar STIKAROVSKÁ; Sáva PEŠÁK; Marcela VLKOVÁ a Jiří LITZMAN

Vydání

Journal of Clinical Immunology, 2012, 0271-9142

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30300 3.3 Health sciences

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 3.382

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14110/12:00059958

Organizační jednotka

Lékařská fakulta

Klíčová slova anglicky

IgA deficiency . common variable immunodeficiency . B-lymphocyte subpopulations

Příznaky

Mezinárodní význam
Změněno: 3. 4. 2013 11:53, Ing. Mgr. Věra Pospíšilíková

Anotace

V originále

Selective deficiency IgA (IgAD) is the most common primary abnormality of immunoglobulin production with unknown pathophysiology. It is genetically related to common variable immunodeficiency (CVID), where besides IgA also IgG and frequently IgM serum levels are decreased. In this study we focused on determination of B-lymphocyte developmental stages and searching for similarities between CVID and IgAD. Materials and Methods Using flow cytometry we determined major lymphocyte subpopulations and Blymphocyte subsets: naive (CD27-IgD+), marginal zone cells (CD27+IgD+), class-switched memory cells (CD27+IgD-), “double-negative” B cells (CD27-IgD-), transitional cells (IgM++CD38++), plasmablasts (CD38+++IgM+ or IgM-), and CD21lowCD38low cells in 80 patients with IgAD, 48 patients with CVID, and 80 control persons. Results Compared to healthy controls, a decrease in the absolute number and frequency of CD4+ cells (both<0.001) was observed in IgAD patients. A decrease in the frequency of switched memory cells (P<0.001), transitional cells (P00.035) as well as plasmablasts (P<0.001) and an increase in the CD21lowCD38low subset (P00.007) was observed in IgAD patients compared to control persons. No significant differences were observed in the remaining B-cell developmental subsets. A decrease in CD27+IgD- (<0.4% of peripheral blood lymphocytes), frequently observed in CVID patients and also previously reported in IgAD, was found in only five patients (6%) with IgAD, two of them being firstdegree relatives of CVID patients. Conclusion Our results show a decrease of terminally differentiated B-lymphocyte subsets in patients with IgAD, similar as previously found in patients with CVID, but these results are less expressed than in CVID patients.