Fc gamma R IIIB polymorphisms: their association with clinical manifestations and autoantibodies in SLE patients from western India.
BACKGROUND
Receptors for the Fc fragment of immunoglobulin G (Fc gamma Rs) represent the link between the humoral and cellular immune responses. Polymorphisms of Fc gamma R, mainly IIA, IIB, IIIA, IIIB have been identified as genetic factors influencing susceptibility to disease or disease course of a prototype autoimmune disease like systemic lupus erythematosus (SLE). Fc gamma alleles may be associated with inefficient removal of apoptotic cells or antigens and hence may be associated with higher risk of SLE.


OBJECTIVE
This study was designed to look for Fc gamma R IIIB polymorphisms of three different alleles, NA1, NA2 and SH in SLE patients and to correlate the distribution of Fc gamma R IIIB genotypes with clinical presentation and autoantibody profile.


METHODS
Eighty SLE patients along with eighty normal individuals were studied. Fc gamma R IIIB polymorphism was tested by allele-specific primer amplification.


RESULTS
The percentage distribution of NA1/NA1, NA1/NA2 and NA2/NA2 was 22.5%, 40% and 37.5%, respectively, among the normal population; and among SLE patients it was 25%, 40% and 35%, respectively. The percentage distribution of SH allele was 68.8% among the normal population, while in SLE patients it was 60%. No statistical difference was found in the distribution of Fc gamma R IIIB genotypes in patients of lupus nephritis and SLE without nephritis (P > 0.05).


CONCLUSIONS
Among SLE patients studied, NA2 was the prominent allele. It was commonly associated with clinical manifestations such as skin rash, arthritis, hematological and immunological disorders. This suggests that the primary involvement of Fc gamma R IIIB NA2 allele is more likely involved with disease susceptibility of SLE.
Department of Autoimmune Disorders, National Institute of Immunohaematology, Indian Council of Medical Research, KEM Hospital, Parel, Mumbai, Maharashtra, India. pradhanv69@rediffmail.com
Vandana
V
Pradhan
Neha
N
Deshpande
Anita
A
Nadkarni
Manisha
M
Patwardhan
Prathamesh
P
Surve
Kanjaksha
K
Ghosh
D000328:Adult; D001323:Autoantibodies; D003430:Cross-Sectional Studies; D005260:Female; D058851:GPI-Linked Proteins; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006304:Health Status; D006801:Humans; D007519:Isoantigens / Q000235:genetics / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000235:genetics* / Q000276:immunology* / Q000503:physiopathology; D008297:Male; D011110:Polymorphism, Genetic; D017452:Receptors, IgG / Q000235:genetics*; D012720:Severity of Illness Index
D001323:Autoantibodies; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D007519:Isoantigens; D017452:Receptors, IgG; C067704:neutrophil-specific antigen NA1, human; C072753:neutrophil-specific antigen NA2; C104384:neutrophil-specific antigen SH