idradenitis suppurativa (HS) is a debilitating, painful chronic inflammatory disease for which the inherent unpredictability with respect to the course of disease and response to treatment poses significant challenges for patients. With sparse epidemiologic data for HS, disease burden has not yet been established. The prevalence of HS has been estimated using claims analyses, examinations, medical record reviews, or patient-administered questionnaires. Most prevalence studies have involved selected samples and/or small cohorts, which limit generalizability. Because of the different data acquisition methods, study settings, and geographic samples in these analyses, prevalence estimates have, not surprisingly, varied significantly across the world. Overall prevalence estimates for HS in Europe and in the United States have ranged from 0.00033% to as high as 4.1%. 1-10 Few adjusted population analyses on which HS prevalence may be accurately estimated have been performed. The true overall prevalence of HS is therefore unknown. The purpose of our study was to establish standardized prevalence estimates for HS in the overall US population and in specific demographic subgroups. Methods Case IdentificationWe performed a retrospective case cohort analysis by querying a multi-institutional data analytics and research platform (Explorys) developed by IBM Watson Health. 11 Clinical information from electronic medical records, laboratories, practice management systems, and claims systems is matched using the single set of Unified Medical Language System ontologies IMPORTANCE The true prevalence of hidradenitis suppurativa (HS) is unknown. OBJECTIVE To establish standardized overall and group-specific prevalence estimates for HS in the United States. DESIGN, SETTING, AND PARTICIPANTSThis retrospective analysis included a demographically heterogeneous population-based sample of more than 48 million unique patients across all US census regions. As of October 27, 2016, a total of 47 690 patients with HS were identified using electronic health record data. MAIN OUTCOMES AND MEASURESStandardized overall point prevalence for HS and sex-, age-, and race-specific prevalence estimates of HS in the general US population. RESULTSOf the 47 690 patients with HS (26.2% men and 73.8% women), the overall HS prevalence in the US population sample was 0.10%, or 98 per 100 000 persons (95% CI, 97-99 per 100 000 persons). The adjusted prevalence in women was 137 per 100 000 (95% CI, 136-139 per 100 000), more than twice that of men (58 per 100 000; 95% CI, 57-59 per 100 000; P < .001). The prevalence of HS was highest among patients aged 30 to 39 years (172 per 100 000; 95% CI, 169-275 per 100 000) compared with all other age groups (range, 15-150 per 100 000; P < .001). Adjusted HS prevalences among African American (296 per 100 000; 95% CI, 291-300 per 100 000) and biracial (218 per 100 000; 95% CI, 202-235 per 100 000) patients were more than 3-fold and 2-fold greater, respectively, than that among white patients (95 per 100 000; 95% CI, 94-9...

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Immunity to viruses must be tightly controlled to avoid pathology. Receptors and ligands of the tumor necrosis factor (TNF) family play important roles in controlling lymphocyte activation and survival during an immune response. The role of specific TNF receptor (TNFR) family members in antiviral immunity depends on the stage of the immune response and can vary with the virus type and its virulence. Here, we focus on five members of the TNFR family that are prominently expressed on CD8(+) T cells during viral infections, namely, 4-1BB (CD137), CD27, OX40 (CD134), GITR, and TNFR2. 4-1BB, CD27, OX40, and GITR have primarily prosurvival roles for CD8(+) T cells during viral infection, although under some circumstances 4-1BB, GITR, or CD27 signals can limit immunity. Although TNFR2 can be costimulatory under some circumstances, its main role in CD8(+) T-cell responses during viral infection appears to be in contraction of the response. Several TNF family ligands are being explored as adjuvants for viral vaccines, and agonistic antibodies to TNFR family members are being investigated for immunotherapy of chronic viral infection alone and in combination with checkpoint blockade. Such therapies will require thorough and specific optimization to avoid pathology induced by hyperstimulation of these pathways.

Although widely studied as a neurotransmitter, T cell–derived acetylcholine (ACh) has recently been reported to play an important role in regulating immunity. However, the role of lymphocyte-derived ACh in viral infection is unknown. Here, we show that the enzyme choline acetyltransferase (ChAT), which catalyzes the rate-limiting step of ACh production, is robustly induced in both CD4+ and CD8+ T cells during lymphocytic choriomeningitis virus (LCMV) infection in an IL-21–dependent manner. Deletion of Chat within the T cell compartment in mice ablated vasodilation in response to infection, impaired the migration of antiviral T cells into infected tissues, and ultimately compromised the control of chronic LCMV clone 13 infection. Our results reveal a genetic proof of function for ChAT in T cells during viral infection and identify a pathway of T cell migration that sustains antiviral immunity.