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A 46-year-old previously healthy female developed flu-like symptoms several days prior to presenting to a local hospital. The patient did not note a recent travel history, specifically denying travel to China. Sick contact exposure was not known. Chest X-ray and computed tomography of the chest showed findings concerning for lobar pneumonia.Subsequent radiology studies showed worsening lung findings along I M A G E 1 Review of the peripheral smear at ×100 magnification shows a nucleated erythroid, A, rare blast, with prominent nucleoli and immature chromatin pattern, B, a left shifted myeloid series with immature promyelocytes and metamyelocyte, C, and occasional monocytes noted, D

Increasing evidence supports an important role for inflammation in all phases of atherosclerosis, from initiation of the fatty streak to final culmination in acute coronary syndromes. Numerous inflammatory biomarkers including cell adhesion molecules, cytokines, chemokines, and acute-phase reactants such as fibrinogen, serum amyloid A, and C-reactive protein (CRP) have been shown to predict cardiovascular (CVD) events. Several prospective studies have shown a consistent and robust relationship between levels of high-sensitivity CRP and the risk of future CVD events. Toll-like receptors are pattern recognition receptors and members of the innate immune system that contribute to inflammation and appear to play key roles in atherosclerosis. Lipoprotein-associated phospholipase A2 may also be an independent CVD risk factor. Psoriasis has been associated with an increasing risk for atherosclerosis, including coronary artery disease and stroke. Patients with psoriasis have a 5-year shorter life expectancy, most frequently due to CVD. Psoriasis is associated with a chronic inflammatory state and with elevated levels of CRP and other inflammatory cytokines and these may play a causative role in the increased risk of psoriatic patients for CVD. Patients with psoriasis may represent an emerging risk population and patients with moderate to severe psoriasis should be screened and aggressively treated for CVD risk factors.

IntroductionInterleukin-22 (IL-22) is a cytokine of IL-10 family with significant proliferative effect on different cell lines. Immunopathological role of IL-22 has been studied in rheumatoid arthritis (RA) and psoriasis. Here we are reporting the functional role of IL-22 in the inflammatory and proliferative cascades of psoriatic arthritis (PsA).MethodFrom peripheral blood and synovial fluid (SF) of PsA (n = 15), RA (n = 15) and osteoarthritis (OA, n = 15) patients, mononuclear cells were obtained and magnetically sorted for CD3+ T cells. Fibroblast like synoviocytes (FLS) were isolated from the synovial tissue of PsA (n = 5), RA (n = 5) and OA (n = 5) patients. IL-22 levels in SF and serum were measured by enzyme linked immunosorbent assay (ELISA). Proliferative effect of human recombinant IL-22 (rIL-22) on FLS was assessed by MTT (3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide, a yellow tetrazole) and CFSE dilution (Carboxyfluorescein succinimidyl ester) assays. Expression of IL-22Rα1 in FLS was determined by western blot.ResultsIL-22 levels were significantly elevated in SF of PsA patients (17.75 ± 3.46 pg/ml) compared to SF of OA (5.03 ± 0.39 pg/ml), p < 0.001. In MTT and CFSE dilution assays, rIL-22 (MTT, OD: 1.27 ± 0.06) induced significant proliferation of FLS derived from PsA patients compared to media (OD: 0.53 ± 0.02), p < 0.001. In addition, rIL-22 induced significantly more proliferation of FLS in presence of TNF-α. IL-22Rα1 was expressed in FLS of PsA, RA and OA patients. Anti IL-22R antibody significantly inhibited the proliferative effect of rIL-22. Further we demonstrated that activated synovial T cells of PsA and RA patients produced significantly more IL-22 than those of OA patients.ConclusionSF of PsA patients have higher concentration of IL-22 and rIL-22 induced marked proliferation of PsA derived FLS. Moreover combination of rIL-22 and TNF-α showed significantly more proliferative effect on FLS. IL-22Rα1 was expressed in FLS. Successful inhibition of IL-22 induced FLS proliferation by anti IL-22R antibody suggests that blocking of IL-22/IL-22R interaction may be considered as a novel therapeutic target for PsA.