CD80 (B7-1) and CD86 (B7-2) expression in multiple sclerosis patients: clinical subtype specific variation in peripheral monocytes and B cells and lack of modulation by high dose methylprednisolone

Autoimmune activation of T cells by central nervous system (CNS)-derived an tigens is hypothesised to underlie neural damage in multiple sclerosis (MS) patients. The role of coreceptor mediated signalling is currently under in vestigation in order to further elucidate the immunopathogenic mechanisms i mplicated and to determine possible targets for immune modulation. We have investigated whether differential coreceptor (B7-1/CD80; B7-2/CD86; CD28) e xpression on circulating lymphocytes and monocytes is (i) a feature of dist inctive clinical subtypes of MS (relapsing-remitting in remission/stable-RR MS; relapsing-remitting in relapse/relapsing-RRMS; primary progressive/PPMS ), (ii) related to disease activity, and (iii) altered by high dose cortico costeroid treatment. CD80(+) B cells were significantly reduced (P<0.05) in PPMS (4.0+/-0.8%) compared with normal subjects (CON) (9.1+/-1.1%), stable -RRMS (6.7+/-0.7%) and relapsing-RRMS (7.8+/-0.9%) patients. Comparatively fewer monocytes from relapsing-RRMS patients expressed CD86 (relapsing-RRMS 50+/-4.9% vs. stable-RRMS 75.1+/-3.4%, PPMS 77.7+/-3.2%, CON 72.1+/-3.6%/P <0.05). Otherwise expression of coreceptors did not vary significantly betw een the groups. A 3-day course of methylprednisolone therapy did not alter coreceptor expression, but did suppress monocyte and B cell HLA-DR expressi on. There is evidence for differential coreceptor expression on circulating B cells and monocytes in MS disease subtypes. The biological significance of these findings is discussed in relation to alternative theories regardin g coreceptor functioning. (C) 1999 Elsevier Science B.V. All rights reserve d.