Glucocorticoid Influence The Expression Of CD21/IgG On AchR-specfic B Cell And The Secretion Of AchR-Ab In Myasthenia Gravis

Objective:This study is aimed to investigate the role of CD21 in the pathogenesis of myathenia gravis (MG) in aspect of antibodies secretion as well as the impact of glucocorticoid therapy on CD21. The serum and peripheral blood mononuclear cell (PBMC) from the generalized myasthenia gravis (gMG) patients before and after glucocorticoid therapy and the healthy controls (NCs) were collected, then the serum concentration of sCD21 and AchR-Ab, the expression of CD21/IgG in peripheral AchR-specified B cells, the level of CD21 mRNA of PBMC were detected, further the relationship between these results were analyzed, so as to offer a theoretical basis about the intervention of CD21 to therapy MGMethods:20 MG patients before and after glucocorticoid therapy and 20 healthy controls (NCs) were investigated by prospective study, the PBMCs was extracted from the peripheral blood. The expression of AchR+CD21+B cells and AchR+IgG+B cells were detected by flow cytomertry, the levels of CD21mRNA in PBMC were detected by real time polymerase chain reaction (RT-PCR) and the serum concentrations of sCD21 and anti-AchR-Ab were detected by ELISA, further the correlation among them were analyzed.Results:(1) Glucocorticoid therapy reduced the expression of AchR+CD21+B cells in gMG patients (before therapy 1.51%±0.81%, after therapy 0.74%±0.45%), and the difference was significant (p<0.01). However, there was no significant difference between gMG patients after glucocorticoid therapy and NCs (0.74%±0.45%,0.53%±0.40%, P>0.05). (2) Glucocorticoid therapy reduced the levels of AchR+IgG+B cells in gMG patients (0.69%±0.46%,0.27%±0.16%), and the difference was significant (p<0.01). However, there was no significant difference between gMG patients after glucocorticoid therapy and NCs (0.27%±0.16%,0.21%±0.12%, P>0.05). (3) Glucocorticoid therapy reduced the levels of serum sCD21 in gMG patients (5.15U/L±1.65U/L,7.10U/L±1.18U/L), and the difference was significant (P<0.05). However, there was no significant difference between gMG patients after glucocorticoid therapy and NCs (7.10 U/L±1.18 U/L,7.88 U/L±1.73 U/L, p>0.05). (4) The expression of CD21mRNA in PBMC was no significant difference between gMG patients before and after glucocorticoid therapy and NCs (respectively, 0.534±0.116 0.548±0.081,0.541±0.091, p>0.05). (5) In anti-AchR-Ab positive gMG patients, the expression of AchR+CD21+B cells was positive correlated with the serum levels of anti-AchR-Ab before and after glucocorticoid therapy (respectively, r=0.864,p<0.01; r=0.537, p<0.05); (6) In anti-AchR-Ab positive gMG patients, the expression of AchR+IgG+B cells in periphery was not significant correlated with the serum levels of AchR-Ab before and after glucocorticoid therapy (respectively, r=0.167, r=0.289; both p>0.05). (7) In anti-AchR-Ab positive gMG patients, the levels of serum sCD21 was negative correlated with AchR-Ab before and after glucocorticoid therapy (respectively, r=-0.556, r=-0.500; both p<0.05).Conclusion:(1) The increased expression of CD21 on AchR specific B cells might stimulate the activation of B cells which lead to the secretion of AchR-Ab.(2) Glucocorticoid therapy inhibited the B cells activation as well as the AchR-Ab secretion by inhibiting the expression of CD21 in AchR specific B cells of gMG patients.