Jaime Pons, Spain

Hospital Universitario Son Espases Immunology

Presenter of 1 Presentation

Poster Display Immune dysregulation & autoimmunity

DECREASED CXCR5 EXPRESSION IN NAÏVE B-CELLS FROM SMB- CVID PATIENTS.

Lecture Time
10:13 - 10:14
Presenter
Room
Poster Area
Date
19.09.2019, Thursday
Session Time
10:00 - 17:00
Board Number
115
Presentation Topic
Immune dysregulation & autoimmunity

Abstract

Background and Aims

B and T cell migration into B-cell follicles depends on the chemokine receptor CXCR5 and its ligand CXCL13. CXCR5 expression on mature B and follicular T cells is essential for T–B encounters and B-cells differentiation into memory or antibody-secreting B-cells.

B-cells differentiation is defective in common variable immunodeficiency disease (CVID) patients.

Methods

Therefore, we studied the expression of the chemokine receptor CXCR5 on total and B-cells subpopulations from smB- CVID patients group. The relationship between the expression of CXCR5 and CD21 in smB- CVID B-cells was also evaluated.

Results

The percentage of CXCR5+ B-cells was lower in smB- CVID patients than controls (85.61% vs. 93.23%; p<0.05). When we compared CXCR5 expression in B-cells subpopulations, differences were restricted to naive B-cells (85.17% vs. 95.33%; p<0.001). No differences were found neither in non-class switched nor in class switched memory B-cells. Percentage of CXCR5- B-cells in smB- CVID patients positively correlated with the percentage of CD21low B cells and percentage of double positive CXCR5+CD21+ B cells was lower in smB- CVID patients than controls (67.11% vs. 90.86%; p<0.001).

Conclusions

We have found an increase of CXCR5- B-cells that correlates with CD19+CD21low subpopulation in smB- CVID patients. CD21low subpopulation is expanded in autoimmune diseases and also in a subgroup of CVID patients with autoimmunity. We hypothesize that CXCR5- naïve B-cells subpopulation in smB- CVID patients might display difficulties to gain access to secondary lymphoid organs and cooperate with Tfh-cells in a negative feedback loop.

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