Hm. Gebel et al., MITOGEN-INDUCED PRODUCTION OF POLYCLONAL IGG IS DECREASED IN WOMEN WITH SEVERE ENDOMETRIOSIS, American journal of reproductive immunology [1989], 29(2), 1993, pp. 124-130
PROBLEM: The etiology and/or pathogenesis of endometriosis may involve
aspects of both humoral and cellular immunity. METHOD: In this invest
igation, we analyzed the ability of B lymphocytes from distinct patien
t groups for production of IgG1, IgG2, and IgG3 following in vitro sti
mulation with polyclonal B-cell mitogens (pokeweed mitogen and Staphyl
ococcus aureus Cowan strain 1) after in vitro stimulation with polyclo
nal B-cell activators. RESULTS: We observed that the in vitro producti
on of IgG1, IgG2, and IgG3 was identical among fertile controls (no en
dometriosis; N = 22), infertile women without endometriosis (N = 22),
infertile women without endometriosis (N = 20) and patietns with stage
1 or 2 endometriosis (N = 31). In contrast, in vitro IgG2 production
was significantly reduced among women with stage 3 or 4 endometriosis
(N = 11) compared to controls (P < 0. 001). CONCLUSION: Since the numb
er of circulating B cells was similar in each patient group studied, t
he reduced production of IgG2 in patients with stage 3 or 4 disease wa
s not merely due to fewer antibody producing cells in those subjects,
and we speculate that the observed decrease in polyclonal IgG2 product
ion among these patients is due to a primary defect. In additional stu
dies, we observed that polyclonal IgG2 production was normal among sta
ge 3 or 4 patients treated with danazol (N = 11), but significantly re
duced in patients treated with gonadotropin releasing hormone agonists
(N = 8). Although not conclusive, these data suggest that danazol may
have the capacity to correct the defective production of polyclonal I
gG2 in patients with severe endometriosis.