Decreased expression of HLA-DR antigens on monocytes in patients with multiple sclerosis

Baxevanis, Constantin N.; Reclos, George J.; Arsenis, Paula; Anastasopoulos, Emmanuel; Katsiyiannis, Anna; Lymberi, Peggy; Matikas, N.; Papamichail, Michail

doi:10.1016/0165-5728(89)90015-5

Cited by 20 publications

(4 citation statements)

References 25 publications

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“…One of these siblings was ICA-positive and presented with type 1 diabetes 6 months later, while the other had active rheumatoid arthritis. Moreover, defective class I1 expression has recently been described by other groups in certain autoimmune diseases including rheumatoid arthritis (2,5 ) , systemic lupus erythematosus (1 7 ) , psoriasis (2 1) and multiple sclerosis (1,13).…”

Section: Discussionmentioning

confidence: 97%

Defective HLA class II expression in monocytes of type 1 diabetic patients

Parkkonen¹,

Hyöty

Huupponen

et al. 1993

APMIS

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Activation of T‐helper cells is modulated by the intensity of HLA class II expression on antigen‐presenting cells. We evaluated whether any abnormalities could be found in the expression of HLA‐DR and ‐DQ molecules on monocytes in type 1 diabetic subjects. DR and DQ molecules were induced by human recombinant interferon‐gamma on cultured peripheral blood monocytes obtained from children with type 1 diabetes (N = 28), their siblings (N = 18) and unrelated healthy controls (N = 21). The response in DQ induction varied considerably between different individuals, but the average responsiveness was significantly lower in patients compared to siblings and unrelated controls. In addition to the diabetic subjects deficient DQ induction was also observed in three siblings. One of them had high levels of islet cell antibodies and presented with diabetes 6 months later, and another had active rheumatoid arthritis. The response in DR induction was also slightly lower in patients than in siblings, but did not differ from that in unrelated controls. The results suggest abnormalities in the regulation of HLA class II expression in type 1 diabetic subjects possibly reflecting the ongoing autoimmune process.

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Section: Discussionmentioning

confidence: 97%

Defective HLA class II expression in monocytes of type 1 diabetic patients

Parkkonen¹,

Hyöty

Huupponen

et al. 1993

APMIS

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“…in patients with septic diseases (26). HLA-DR expression on circulating monocytes varies as a function of disease activity in patients with multiple sclerosis (27), and the active form of this disease is characterized by reduced HLA-DR density on blood monocytes (28). There were, however, no changes in the expression of HLA-DR antigen on blood monocytes of Parkinson's disease patients in comparison to control groups.…”

Section: Discussionmentioning

confidence: 99%

Parkinson's disease and immunological abnormalities: increase of HLA-DR expression on monocytes in cerebrospinal fluid and of CD45RO+ T cells in peripheral blood

Fiszer

Mix

Fredrikson

et al. 2009

Acta Neurologica Scandinavica

123

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The etiology of Parkinson's disease is mainly unknown. Immune abnormalities have been described, but the cause of such abnormalities has not been resolved. We examined by two‐colour flow cytometry HLA‐DR antigen expression on monocytes from cerebrospinal fluid (CSF) and blood and, moreover, lymphocyte subpopulations (CD4+ CD45RO+, CD4+ CD45RA+, CD8+ CD11b+high) in peripheral blood from patients with Parkinson's disease compared with age‐matched patients with other neurological diseases (OND) and tension headache. We found higher HLA‐DR expression on CSF monocytes compared with blood monocytes. This difference was restricted to Parkinson's disease patients. T helper cell analysis revealed a decreased percentage of CD45RA+“naive” and an increased percentage of CD45RO+“memory” T cell subset from CD4+ T cells in peripheral blood of patients with Parkinson's disease compared with patients with tension headache. The proportions of CD8+ CD11b+high“suppressor” T cells remained unchanged, among the three patient groups compared. A selective loss of CD4+ CD45RA+ cells, previously observed in diseases like multiple sclerosis and Down's syndrome as compared with healthy controls suggests a common immunological abnormality in neurological disorders.

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“…The increase in HLA-DR on monocytes at 6 months already described in our previous work [7] was confirmed in the present study and was even more evident at 12 months. The increase in treated MS patients could be considered as a compensation mechanism, if, as reported by Baxevanis et al [2] and Ransohoff et al [15], there is less HLA-DR expression on the surface of monocytes in MS patients than in those of healthy controls. In this respect, reports in the literature are conflicting [17], but the present study seems to suggest that this may actually be the case.…”

Section: Discussionmentioning

confidence: 91%

Immunological effects of in vivo interferon-β 1b treatment in ten patients with multiple sclerosis: a 1-year follow-up

Gelati

Corsini

Dufour

et al. 1999

Journal of Neurology

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Ten patients with multiple sclerosis and treated with interferon-beta1b (IFN-beta1b) were followed-up for 1 year with quantitation of serum VCAM-1 and ICAM-1 levels, mean fluorescence intensity of HLA-DR, VLA-4, CD11a, and CD18 on peripheral blood monocytes and lymphocytes, and adhesion of peripheral blood monocytes and CD45+ cells on endothelial cell monolayers. Adhesion molecule expression and adhesion of peripheral blood monocytes to endothelium were also monitored in healthy controls. No differences in adhesion were detected between MS patients before treatment and healthy controls, while after 1 year a marked decrease in the number of monocytes and mononuclear cells adhering to human umbilical vein endothelial cell monolayers was observed in patients treated with IFN-beta1b. After 1 year of treatment a significant increase in HLA-DR on peripheral blood monocytes was also detected. Our findings regarding lowered adhesion add information to available evidence of the mechanisms of action of IFN-beta1b in MS.

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Decreased expression of HLA-DR antigens on monocytes in patients with multiple sclerosis

Cited by 20 publications

References 25 publications

Defective HLA class II expression in monocytes of type 1 diabetic patients

Defective HLA class II expression in monocytes of type 1 diabetic patients

Parkinson's disease and immunological abnormalities: increase of HLA-DR expression on monocytes in cerebrospinal fluid and of CD45RO+ T cells in peripheral blood

Immunological effects of in vivo interferon-β 1b treatment in ten patients with multiple sclerosis: a 1-year follow-up

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