CD200/CD200 receptor axis in psoriasis vulgaris

Abstract

Background Psoriasis is a chronic inflammatory multisystem disease with imbalance between the Th17 and T regulatory sub-populations. CD200/CD200R is an anti-inflammatory/immune-suppressive axis that might contribute to its pathogenesis given its relation to the Tregs induction. The current study aimed to investigate the status of the CD200/CD200R axis in the blood of psoriasis vulgaris patients versus healthy controls. Methods In this comparative cross sectional study, the blood levels of sCD200 and CD200R levels were measured in 25 psoriasis vulgaris patients and an age and sex matched 25 healthy controls using ELISA and flow-cytometry respectively. Their levels were tested for correlation to disease severity. Results sCD200 was significantly higher while CD200R was significantly lower in psoriasis vulgaris patients than in controls. They did not correlate to each other or to psoriasis severity although they differed significantly among cases of different severities. Conclusion Aberrant expression of CD200/CD200R might play a role in psoriasis vulgaris pathophysiology and disease severity. It might constitute a future target of therapy, but cannot be used as a marker of disease severity.

CD200 and CD200R Expression on Peripheral Blood Lymphocytes and Serum CD200 Concentration as a New Marker of Endometriosis

“…However, its role as a controller of inflammatory activity in EMS seems to be reduced, because the inhibitory signal of CD200 was transduced by activating the intracellular-signaling motifs of its receptor. Deficient expression of CD200R blocks the effects of the upregulated ligand, resulting in the failure of T cell polarization into a Treg subpopulation and the development of Th17, both involved in the pathogenesis of EMS [ 17 , 18 , 42 ]. Similar findings were reported by Elshal et al [ 43 ] for Th cells in inflammatory bowel disease (IBD) in pediatric patients.…”

“…Another mechanism involves the upregulation of deposits of indoleamine-pyrrole 2,3-dioxygenase (IDO), which modulates macrophage differentiation into the tolerogenic phenotype. Its overexpression may induce the depletion of local tryptophan and the production of kynurenines—tryptophan metabolites that are powerful inducers of apoptosis in cluster of differentiation 4-positive (CD4+) T cells [ 17 , 18 ]. IDO expression promotes the immunosuppressive profile of DCs and stimulates the anergic status of effector T cells [ 18 ].…”

PD1hi CD200hi CD4+ exhausted T cell increase immunotherapy resistance and tumour progression by promoting epithelial–mesenchymal transition in bladder cancer

“…The imbalance of Tregs/Th17 cells can be caused by the CD200–CD200R signalling pathway, which induces Treg generation and prevents Th17 differentiation, thus resulting in immune tolerance 63,64 . Moreover, the activation of the CD200/CD200R signalling pathway is also a key contributor to the Treg phenotype 65,66 . In light of the above studies, we hypothesized that PD1 hi CD200 hi CD4 + exhausted T cells may have the traits of Tregs.…”

“… 63 , 64 Moreover, the activation of the CD200/CD200R signalling pathway is also a key contributor to the Treg phenotype. 65 , 66 In light of the above studies, we hypothesized that PD1 hi CD200 hi CD4 + exhausted T cells may have the traits of Tregs. Next, our results indicated that patients with high proportions of PD1 hi CD200 low CD4 + exhausted T cells had an excellent prognosis following immunotherapy, whereas those with high proportions of PD1 hi CD200 hi CD4 + exhausted T cells demonstrated immune tolerance.…”

Reduced cutaneous CD200:CD200R1 signaling in psoriasis enhances neutrophil recruitment to skin

“…We show reduced CD200 in PN skin, similar to previous RNAseq data. 25 Conversely, recent studies showed elevated soluble CD200 in psoriasis patient blood, 45 , 46 tempting speculation that the reduced cell‐associated CD200 in skin, may be caused by enhanced CD200 cleavage. However, the reduced CD200 mRNA levels seen (Figure 1A and previously 25 ), suggest that reduced CD200 in skin is due (at least in part) to decreased transcription.…”