Anti-CD4 monoclonal antibody, clone KEN-4

Background Information about the impact of HIV coinfection on clinical characteristics of COVID-19 patients remains limited. Methods Maximum body temperatures, fever duration, chest CT and viral shedding, lymphocyte counts, and titer of SARS-CoV-2 antibody were compared between COVID-19 patients with and without HIV infection in Zhongnan Hospital of Wuhan University from January 20th to February 14th, 2020. Results Compared with 53 COVID-19 patients without HIV infection, the patients with SARS-CoV-2 and HIV coinfection had higher maximum body temperatures (38.7 degrees C vs 37.6 degrees C, P = 0.044), longer duration of fever (8.7 +/- 4.5 vs 4.2 +/- 2.1 days, P = 0.038), longer time to have improvement of chest CT images (22 vs 15 days from the onset of illness, P = 0.011), lower level of SARS-CoV-2 IgG (5.11 +/- 32.33 vs 37.45 +/- 15.48 AU/ml, P = 0.042). However, no statistically significant difference of duration of SARS-CoV-2 shedding in the two groups was found (12.3 +/- 2.6 vs 13.4 +/- 2.4 days, , P = 0.813). Conclusion Lower level of CD4(+) T lymphocyte counts caused by HIV infection itself might be one of reasons for relatively weak ability to produce SARS-CoV-2 specific antibodies. The effects of anti-HIV drugs in prevention and treatment of COVID-19 appears to be limited.

Pemphigus vulgaris (PV) and bullous pemphigoid (BP) are autoantibody-mediated diseases clinically characterized by blisters and erosions of skin and/or mucous membranes. Immune imbalance and antibody generation are the key pathologies of autoimmune bullous diseases. Recently, a large number of studies have shown that T cell subsets, which are critical players in autoimmunity, exhibit a range of abnormalities and drive immunopathogenesis and skin inflammation in PV and BP. T helper (Th)1 cells mediate pro-inflammatory or immune responses through IFN-gamma and Th2-derived cytokines, such as IL-4, can promote B cell proliferation, antibody production and immunoglobulin class-switching. Th17 cells promote inflammatory response and skin damage, while regulatory T cells suppress autoreactive CD4(+) T cell activation and help control inflammation. T follicular helper cells cross-talk with B cells and facilitate autoantibody production. In this review, we discuss the immune features of PV and BP, with a focus on the aberrations in T cell subsets, such as Th1 cells, Th2 cells, Th17 cells, regulatory T cells, T follicular helper cells, CD8(+) T cells, gamma delta T cells and resident memory T cells in the pathogenesis of PV and BP. Improved understanding of biological and immunological functions of T cell subsets in patients with autoimmune skin disorders will offer unique opportunities for the recognition of treatment targets for these complex diseases.