Sachiko Hirose 1, Qingshun Lin 1, Mareki Ohtsuji 1, Hiroyuki Nishimura 1, J Sjef Verbeek 1 , Int Immunol. 2019 Oct 16;31(11):687-696
Tag: autoimmune disease
Monocyte subsets involved in the development of systemic lupus erythematosus and rheumatoid arthritis
AbstractMonocytes are evolutionally conserved innate immune cells that play essential roles for the protection of the host against pathogens and also produce several inflammatory cytokines. Thus, the aberrant functioning of monocytes may affect not only host defense but also the development of inflammatory diseases. Monocytes are a heterogeneous population with phenotypical and functional differences. Most recent studies have shown that monocytes are divided into three subsets, namely classical, intermediate and non-classical subsets, both in humans and mice. Accumulating evidence showed that monocyte activation is associated with the disease progression in autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). However, it remains to be determined how monocytes contribute to the disease process and which subset is involved. In this review, we discuss the pathogenic role of monocyte subsets in SLE and RA on the basis of current studies by ourselves and others to shed light on the suitability of monocyte-targeted therapies in these diseases.
In vivo modulation of leukocyte trafficking receptor following therapeutic purging of myeloid cells: implications for treatment of HIV infection and other immune disorders
Priscilla Biswas Barbara Mantelli Alberto Beretta Clinical Immunology 109 (2003) 355–358 DOI: 10.1016/j.clim.2003.07.001
Therapeutic purging of myeloid cells (monocytes and granulocytes) (MYP) has been proposed as a treatment of severe inﬂammatoryconditions like ulcerative colitis and rheumatoid arthritis. Although direct purging of inﬂammatory cells contributes to its efﬁcacy, the precise mechanism of action is still unclear. We have tested MYP in a pilot study on 12 patients with chronic HIV infection, of whom 6 underwent MYP. Three/6 MYP patients and none of the controls displayed a strong and long-lasting decrease of cells expressing CXCR3,a major chemokine receptor responsible for trafﬁcking of inﬂammatory cells. In these three patients, the number of circulating CD4 T cells increased during treatment. The data provide a rational for the use of MYP as a therapeutic tool acting via the modulation of immune cell trafﬁcking
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