Pan-pox-specific T-cell responses in HIV-1-infected individuals after JYNNEOS vaccination.

People living with human immunodeficiency virus (HIV) are the individuals most affected by the current Monkeypox virus outbreak that was first announced in May 2022. Here we report Pan-pox-specific T-cell responses in a cohort of HIV-1-infected individuals after receiving the nonreplicative, attenuated smallpox vaccine JYNNEOS from Bavarian Nordic. Intradermal (i.d.) and subcutaneous (s.c.) vaccination was safe without major side effects. Dose-sparing i.d. vaccination was superior to s.c. vaccination and promoted T-cell polyfunctionality, and the expression of the gut-homing marker α4ß7 integrin on lymphocytes. HIV-1-infected individuals with CD4 T-cell counts ≤500/mm3 blood required at least a booster vaccination to exhibit efficient virus-specific T-cell responses. The magnitude of the Th1 response after this booster directly correlated with the CD4 T-cell count of the vaccinees. Further studies with a larger number of participants are warranted to confirm and expand our observations.

Interleukin-32 in Pathogenesis of Atopic Diseases: Proinflammatory or Anti-Inflammatory Role?

Atopic diseases, such as atopic dermatitis (AD), allergic asthma (AA), and allergic rhinitis (AR), are increasingly becoming a worldwide issue. This atopic triad originates at an early age and on a multifactorial basis, causing significant discomfort to susceptible individuals. The global case number is now reaching new highs, so exploring immune system regulation and its components is becoming critical. One cytokine, interleukin-32 (IL-32), is involved in inflammation and regulation of the immune system. It has nine isoforms that show varying degrees of expression, both intracellularly and extracellularly. IL-32 is secreted by immune cells, such as monocytes, macrophages, natural killer cells, and T cells, and by nonimmune cells, including fibroblasts, keratinocytes, and endothelial cells. Its production is regulated and augmented by microorganisms, mitogens, and other cytokines. Early studies demonstrated that IL-32 was an immune regulator that functioned to protect against inflammatory diseases, including AD, AA, and AR, and proposed a proinflammatory role for IL-32 in immune regulation and symptom exacerbation. However, several later reports suggested that IL-32 is downregulated in inflammatory diseases and exerts an anti-inflammatory effect. This review article focuses on recent findings regarding the detrimental and protective roles of IL-32 in development and management of inflammatory diseases. The exact role of IL-32 in AD, AA, and AR still remains to be elucidated. Future research should explore new avenues of IL-32 functionality in human inflammatory diseases.