Differences Observed in Monocyte Phenotype From Patients With Systemic Lupus Erythematosus and Rheumatoid Arthritis

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Differences Observed in Monocyte Phenotype From Patients With Systemic Lupus

Erythematosus and Rheumatoid Arthritis

02/27/2004 08:23:00 AM

By Jill

Monocytes from patients with systemic lupus erythematosus (SLE) or

rheumatoid arthritis (RA) display significantly altered phenotypes compared

with those from healthy individuals, which may be related to differing

cytokine profiles of the diseases, according to a British study.

Immunoglobulin G-containing immune complexes (IC) are central to the

immunopathology of SLE, and may also play a role in the pathogenesis RA. The

interaction between IC and monocytes is affected by the expression of Fc

(gamma) and complement receptors, and evidence suggests that cytokines may

modify their relative expression on these cells. Cytokines also may alter

the expression of adhesion molecules such as ICAM-1, a mediator of

potentially proinflammatory leucocyte-endothelial interactions. However,

information regarding in vivo expression of specific Fc(gamma) and

complement receptors in SLE or RA is scant. Researchers led by Dr. Alastair

L. Hepburn of Hammersmith Hospital, London, investigated receptor surface

expression on SLE and RA monocytes, the relationship between expression and

clinical disease activity, and whether steroid therapy influences

expression. The study included 30 SLE patients, 25 RA patients, and 25

healthy control subjects. Twenty-two SLE patients and 9 RA patients were

taking prednisolone. Blood samples obtained from participants were analysed

to determine monocyte phenotype, surface expression of Fc(gamma) receptors

RI (CD64), RII (CD32) and RIII (CD16), complement receptors CR1 (CD35) and

CR3 (CD11b/CD18), and adhesion molecules ICAM-1 (CD54) and CD11a (LFA-1).

All monocytes were found to express Fc(gamma) RI and RII. No significant

difference was observed in expression of Fc(gamma)RI on SLE or RA monocytes

compared with controls, but expression of Fc(gamma)RII was reduced on SLE

monocytes compared with controls and RA patients ([P = .002). Although no

significant difference was observed in Fc(gamma)RI or RIII expression on SLE

monocytes compared with healthy controls, expression of Fc(gamma)RIII was

increased on RA monocytes (P = .01). The expression of CR3 was increased on

RA monocytes compared to controls (P = .002). CR1 expression was increased

on monocytes from RA patients with active disease, but not those with

inactive disease. No difference was found between groups in the expression

of CD11a. Conversely, ICAM-1 expression was decreased on SLE monocytes (P =

..002). High-dose prednisolone therapy was associated with lower expression

of both CD11a and ICAM-1 on monocytes. The researchers suggest that the

balance of pro- and anti-inflammatory cytokines is likely to influence the

degree of inflammation and clinical phenotype in chronic inflammatory

diseases. " One of the many contributing mechanisms for this may be the

modification of monocyte phenotype by cytokines, activation in the

circulation by IC, enhanced adhesion and recruitment to sites of tissue

inflammation, " they said. " These effects differ between SLE and RA and may

be modified by therapy including treatment with corticosteroids. "