A regulatory role for CD72 expression on B cells in systemic lupus erythematosus.
BACKGROUND
B regulatory cells and their regulatory products/markers, such us semaphorin 3A (sema3A) and its receptor NP-1, FcγIIB, IL-10, and others, act at the very base of self-tolerance, maintenance, and prevention of autoimmune disease development.


OBJECTIVE
The aim of the present study was to assess the involvement of CD72, a regulatory receptor on B cells, in systemic lupus erythematosus (SLE). In addition, the potential of soluble sema3A in enhancing the expression of CD72 on B cells of SLE patients was investigated.


RESULTS
CD72 expression on activated B cells of SLE patients was significantly lower than that of normal controls. This lower expression of CD72 in SLE patients correlated inversely with SLE disease activity and was associated with lupus nephritis, the presence of anti-dsDNA antibodies, and low levels of complement. Co-culture of purified B cells from healthy controls with condition-media containing recombinant sema3A resulted in significant enhancement of CD72. Similar enhancement of CD72 on activated B cells from SLE patients, though significant, was still lower than in normal individuals.


CONCLUSIONS
The lower expression of CD72 on activated B cells from SLE patients correlates with SLE disease activity, lupus nephritis, the presence of anti-dsDNA antibodies, and low levels of complement. The improvement of CD72 expression following the addition of soluble semaphorin 3A suggests that CD72 may be useful as a biomarker to be followed during the treatment of SLE.
Division of Allergy and Clinical Immunology, Bnai Zion Medical Center, Haifa, Israel; Ruth & Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Zahava
Z
Vadasz
Division of Allergy and Clinical Immunology, Bnai Zion Medical Center, Haifa, Israel; Ruth & Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Tharwat
T
Haj
Rheumatology Unit, Rambam Medical Center, Haifa, Israel; Ruth & Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Alexandra
A
Balbir
Division of Allergy and Clinical Immunology, Bnai Zion Medical Center, Haifa, Israel; Ruth & Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Regina
R
Peri
Rheumatology Unit, Bnai Zion Medical Center, Haifa, Israel; Ruth & Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Itzhak
I
Rosner
Rheumatology Unit, Bnai Zion Medical Center, Haifa, Israel; Ruth & Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Gleb
G
Slobodin
Division of Allergy and Clinical Immunology, Bnai Zion Medical Center, Haifa, Israel; Ruth & Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Aharon
A
Kessel
Division of Allergy and Clinical Immunology, Bnai Zion Medical Center, Haifa, Israel; Ruth & Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel. Electronic address: elias.toubi@b-zion.org.il.
Elias
E
Toubi
D000293:Adolescent; D000328:Adult; D000974:Antibodies, Antinuclear / Q000276:immunology*; D015703:Antigens, CD / Q000276:immunology* / Q000378:metabolism; D000944:Antigens, Differentiation, B-Lymphocyte / Q000276:immunology* / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D060151:B-Lymphocytes, Regulatory / Q000276:immunology; D015415:Biomarkers / Q000378:metabolism; D005260:Female; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008181:Lupus Nephritis / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D040121:Semaphorin-3A / Q000276:immunology*; D055815:Young Adult
D000974:Antibodies, Antinuclear; D015703:Antigens, CD; D000944:Antigens, Differentiation, B-Lymphocyte; D015415:Biomarkers; C064228:CD72 protein, human; C108639:SEMA3A protein, human; D040121:Semaphorin-3A
Autoimmunity; CD72; Regulation; SLE