Severe drug-associated colitis with Crohn's features in setting of ixekizumab therapy for chronic plaque psoriasis.

Background: Ixekizumab is monoclonal antibody targeted against interleukin-17 (IL-17) and has been approved for use in chronic plaque psoriasis. Despite its efficacy in treating psoriasis, concerns have been raised regarding Ixekizumab's potential to induce and exacerbate inflammatory bowel disease (IBD).

Case Presentation: Here we report the new onset of severe drug-associated colitis with surgical complications in a 45-year-old male patient who was receiving Ixekizumab therapy for chronic plaque psoriasis.

Use of Non-Selective Beta-Blocker for Refractory Stomal Variceal Hemorrhage.

Bleeding stomal varices are often difficult to manage given the comorbidities that are associated with their presentation. Here, we report a case of a 62-year-old female with stomal variceal hemorrhage in the setting of chronic portal vein thrombosis who was ineligible for transhepatic intrajugular portosystemic shunt or surgery as a result of her challenging anatomy and peri-operative risks. Despite coil embolization, this patient experienced refractory bleeds which ceased following the initiation of a non-selective beta-blocker (NSBB).

Fas/FasL-independent activation-induced cell death of T lymphocytes from HIV-infected individuals occurs without DNA fragmentation.

We assessed the effects of activation with phorbol myrystic acetate (PMA) and ionomycin on peripheral blood mononuclear cells (PBMC) from HIV-infected individuals by (51)Cr release, propidium iodide (PI) uptake, electron microscopy, and DNA analysis. Up to 70% (51)Cr release was induced from PBMC of HIV-infected individuals, versus up to 26% (51)Cr release from PBMC of non-HIV-infected volunteers. Flow cytometry identified mostly T cells undergoing activation-induced cell death (AICD).

Human immunodeficiency virus type 1 replication, immune activation, and circulating cytotoxic T cells against uninfected CD4+ T cells.

Cytotoxic T lymphocytes (CTL) that kill uninfected activated CD4+ T cells can be induced in vitro by stimulating CD8+ T cells with activated autologous CD4+ T cells. Similar CTL have been detected in circulating T cells from human immunodeficiency virus type I (HIV)-infected individuals. To define the in vivo correlates of this CTL activity, we studied plasma beta-2 microglobulin and HIV RNA levels, T-lymphocyte subset counts, and expression of CD28 on CD8+ T cells concurrently with circulating CTL activity against uninfected CD4+ T cells in 75 HIV-infected individuals at different stages of disease progression.

Functional and genetic integrity of the CD8 T-cell repertoire in advanced HIV infection.

Background: HIV-specific cytotoxic T lymphocytes (CTL) can restrict HIV replication in acute and chronic infection, but disease progression occurs in parallel with declining CTL activity. An understanding of why CTL fail to control HIV replication might reveal important mechanisms of disease progression and enhance prospects for developing effective CTL-based immunotherapies.

Objectives: To investigate the functional integrity, T-cell repertoire diversity, and HIV reactivity of CD8 T lymphocytes in individuals with advanced HIV infection.