Vanishing cerebral vasculitis in a patient with Lewy pathology

Immune-mediated mechanisms are involved in the pathogenesis of both cerebral vasculitis and Parkinson’s disease（PD, brainstem-predominant Lewy pathology）, but the presentation of cerebral vasculitis with comorbid Lewy pathology has not yet been reported. Here we present a case of pathologically confirmed vasculitis in a 73-year-old male patient whose postmortem examination revealed Lewy pathology diagnostic of PD. This case study suggests a comorbidity of cerebral vasculitis and Lewy pathology, as well as potential pathogenic interactions between these two disorders with immune-mediated mechanisms.

The influence of innate and adaptative immune responses on the differential clinical outcomes of leprosy

Leprosy is a chronic infectious disease caused by Mycobacterium leprae.According to official reports from 121 countries across five WHO regions,there were 213899 newly diagnosed cases in 2014.Although leprosy affects the skin and peripheral nerves,it can present across a spectrum of clinical and histopathological forms that are strongly influenced by the immune response of the infected individuals.These forms comprise the extremes of tuberculoid leprosy(TT),with a M.leprae-specific Th1,but also a Th17,response that limits M.leprae multiplication,through to lepromatous leprosy(LL),with M.leprae-specific Th2 and T regulatory responses that do not control M.leprae replication but rather allow bacterial dissemination.The interpolar borderline clinical forms present with similar,but less extreme,immune biases.Acute inflammatory episodes,known as leprosy reactions,are complications that may occur before,during or after treatment,and cause further neurological damages that can cause irreversible chronic disabilities.This review discusses the innate and adaptive immune responses,and their interactions,that are known to affect pathogenesis and influence the clinical outcome of leprosy.

CD4^+ T cell-mediated presentation of non-infectious HIV-1 virion antigens to HIV-specific CD8^+ T cells

Background The mechanism of chronic immune activation and impairment of HIV-specific immune responses during chronic infection is not fully understood. However, it is known that high immune activation leads to more rapid progression to AIDS. We hypothesize that CD4^＋ T cell-mediated viral antigen presentation contributes to this pathologic immune activation in HIV-infected individuals. Methods HIV-specific T cells, responding to noninfectious HIV-1 virions as antigen, were measured by flow cytometric assays. These experimental conditions reflect the in vivo condition where noninfectious HIV-1 represents more than 99% of the antigens. Results CD4^＋ T cells purified from HIV-infected individuals were capable of cross presenting exogenous noninfectious HIV-1 virions to HIV-1-specific CD8^＋ T cells. Cross presentation required the entry of HIV-1 to CD4^＋ T cells and antigen translocation from endoplasmic reticulum to the Golgi complex. Blocking CD4^＋ mediated activation of HIV-specific CD8^＋ T cells and redirecting the viral antigens to antigen presenting cells improved HIV-specific T cell responses. Contusions One possible cause of chronic immune activation and impairment of HIV-1 specific T cell responses is represented by HIV-1 harboring CD4^＋ T cells cross presenting HIV-1 antigen to activate CD8^＋ T cells. This new mechanism provides the first evidence that cross presentation of noninfectious HIV-1 virions play a role in the immunopathogenesis of HIV-1 infection.