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Frontiers | An Update on Protective Effectiveness of Immune Responses After Recovery From COVID-19

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exhibits variable immunity responses among hosts based on symptom severity. Whether immunity in recovered individuals is effective for avoiding reinfection is poorly understood. Determination of immune memory status against SARS-CoV-2 helps identify reinfection risk and vaccine efficacy. Hence, after recovery from COVID-19, evaluation of protective effectiveness and durable immunity of prior disease could be significant. Recent reports described the dynamics of SARS-CoV-2 -specific humoral and cellular responses for more than six months in convalescent SARS-CoV-2 individuals. Given the current evidence, NK cell subpopulations, especially the memory-like NK cell subset, indicate a significant role in determining COVID-19 severity. Still, the information on the long-term NK cell immunity conferred by SARS-CoV-2 infection is scant. The evidence from vaccine clinical trials and observational studies indicates that hybrid natural/ ....

Eastern Cape , South Africa , Western Cape , Saudi Arabia , United Kingdom , South Korea , Free State , Yunbao Pan , Paige Lawrence , Zhengm Tim , Cohen Tervaert , Cullym Exosome , Jernbom Falk , Nasrin Shokrpour , Shiraz University Of Medical Science , Health Sci , Terminal Differentiation Of Plasma Cells In Health , Shiraz University Of Medical Sciences , Development Of Clinical Research Nemazee Hospital , S Specific Igg , Natural Immunity , Vaccine Immunity , Shiraz University , Medical Science , Medical Sciences , Clinical Research ,

Frontiers | The One That Got Away: How Macrophage-Derived IL-1β Escapes the Mycolactone-Dependent Sec61 Blockade in Buruli Ulcer

Buruli ulcer (BU), caused by Mycobacterium ulcerans, is a devastating necrotizing skin disease. Key to its pathogenesis is mycolactone, the exotoxin virulence factor that is both immunosuppressive and cytotoxic. The discovery that the essential Sec61 translocon is the major cellular target of mycolactone explains much of the disease pathology, including the immune blockade. Sec61 inhibition leads to a loss in production of nearly all cytokines from monocytes, macrophages, dendritic cells and T cells, as well as antigen presentation pathway proteins and costimulatory molecules. However, there has long been evidence that the immune system is not completely incapable of responding to M. ulcerans infection. In particular, IL-1beta was recently shown to be present in BU lesions, and to be induced from M. ulcerans-exposed macrophages in a mycolactone-dependent manner. This has important implications for our understanding of BU, showing that mycolactone can act as the “second signal” for ....

United States , Western Australia , Le Bon , Scandj Rheumatol , Rheumatol Oxford , M Ulcerans Mycolactone Cytotoxicity , Pedrosaj Mycolactone , Waal Malefyt , Sarpong Duah , Rajko Reljic , Van Haver , Van Puyenbroeck , Thyet Mycolactone , Mycolactone Polyketide Synthases , Prof Pamela Small University Of Knoxville , Riverside Research Ethics Committee , Kennedy Institute Trustees , Wellcome Trust Investigator Award In Science , Streptomycin For Limited Buruli Ulcer Lesions , Prof Yoshito Kishi Harvard University , Lancet Glob Health , Dr Justice Boakye Appiah St George University London , West Africa , Immune Response , Buruli Ulcer , Wellcome Trust Investigator Award ,