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Coronavirus disease 2019 (COVID-19) is a new human infectious disease. The etiology for this outbreak is a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Thus far, related research on COVID-19 is still in preliminary stage. This paper summarized the latest outcomes of corresponding study from Chinese centers and clarified the hematopoietic abnormality caused by SARS-CoV-2 and potential mechanism. Lymphopenia was common in the early stage after the onset of COVID-19. A significant decrease was observed in peripheral CD4+ and CD8+ T lymphocytes. As the illness progressed, neutrophilia emerged in several cases, and patients with severe critical pulmonary conditions showed higher neutrophils than common type. Thrombocytopenia was resulting from the consumption and/or the reduced production of platelets in damaged lungs. Anemia was not observed notably, but the decrease in hemoglobin was frequent. The activation of monocyte-macrophage system aggravates the immune damage of lung and other tissues, which leads to the increase of D-dimer, prothrombin time, and platelet consumption. [ABSTRACT FROM AUTHOR]

Linkage to care (LTC) and initiation of antiretroviral therapy (ART) are key components in the longitudinal care cascade for people living with HIV. Many strategies to optimize these stages of HIV care have been implemented, though there is a paucity of analyses comparing the outcomes of these efforts in low- and middle-income countries. We conducted a systematic review of studies assessing interventions along all stages of the HIV care continuum published between 2008 and 2020. A comprehensive search strategy reviewed five electronic databases to capture studies assessing HIV testing, LTC, ART initiation, ART adherence, and viral suppression. Of the 388 articles that met the inclusion criteria, 78 described interventions for improving LTC/ART initiation. Efforts focused on empowering patients through integrative approaches generally yielded more substantive results compared to provider-initiated non-adaptive LTC interventions or cash incentives. Specifically, tailoring care and incorporating ART initiation into existing infrastructures, such as maternal clinics, had a high impact across settings. Moreover, strategies such as home-based HIV counseling and testing (HBHCT) appear to be most effective when implemented in tandem with other approaches including motivational counseling and point-of-care CD4 testing. [ABSTRACT FROM AUTHOR]

Objective: Our preview study found that CCR5 blockade combined with cyclosporine A could attenuate the severity of liver GVHD. But the potential immunological mechanisms have not yet been explored. So our present study was designed to clarify the potential immunological mechanisms in mouse models after allo-HSCT. Methods: Firstly, we detected donor T cells homing to target organs, and analyzed the specific effector subsets in liver. Additionally, we assessed antigen-presenting cells (APCs), especially DCs and CD4 T cells differentiation in secondary lymphoid organs. Results: Data showed that MVC combined with CsA reduced donor T cells migration to target organs in vivo. MVC and CsA treatment reduced the amount of donor T cells in the absolute numbers, also in donor CD4 and CD8 T cells by targeting at CCR5. And MVC co-injected with CsA was capable of slightly suppressing DC maturation, and reduced the percentage of Th1 and Th17 mainly by noncompetitive combination of CCR5. Conclusion: Combined use of MVC and CsA was effective in attenuating liver GVHD in murine model. It can suppress DC maturation, affect T cells differentiation, and reduce donor T cells homing to target organs. This may offer a novel therapeutic perspective approach for clinical liver GVHD after allo-HSCT. [ABSTRACT FROM AUTHOR]

Objective: To investigate whether Shen-Fu Injection (参附注射液, SFI) reduces post-resuscitation immune dysfunction in a porcine model of cardiac arrest by modulating apoptosis of regulatory T lymphocytes (Treg) in the spleen. Methods: After 8-min untreated ventricular fibrillation and 2-min basic life support, 24 pigs were divided into 3 groups with a random number table, i.e. SFI group, epinephrine (EP) group, and saline (SA) group (8 in each group), which received central venous injection of SFI (1.0 mL/kg), EP (0.02 mg/kg) and SA, respectively. The same procedure without CA initiation was achieved in the sham-operated (sham) group ( n=6). After successful return of spontaneous circulation (ROSC), apoptosis rate of splenic Treg was detected by flow cytometry; and the mRNA expression of forkhead/winged helix transcription factor (Foxp3) of splenic Treg was detected by real time-polymerase chain reaction; and the levels of interleukin-4 (IL-4) and interferon-γ (IFN-γ) in porcine splenic Treg were detected by using enzyme-linked immunosorbent assay (ELISA). Results: Compared with the sham group, the apoptosis rate of Treg was significantly decreased, and the levels of Foxp3 mRNA expression, IFN-γ, IL-4 and IFN-γ/IL-4 were increased in the SA group ( P<0.05 or P<0.01). Compared with the EP and SA groups, SFI treatment increased the apoptosis rate of Treg and reduced the levels of Foxp3 mRNA expression, IFN-γ and IFN-γ/IL-4 ( P<0.05). Conclusions: SFI has signifificant effects in attenuating post-resuscitation immune dysfunction by modulating apoptosis of Treg in the spleen. [ABSTRACT FROM AUTHOR]

Certain genotypic combinations of killer-cell immunoglobulin-like receptors (KIR) and human leukocyte antigens (HLA) have been associated with favourable outcomes after exposure to human immunodeficiency virus in Caucasoid and African populations. Human immunodeficiency virus (HIV) infection is characterized by a rapid exhaustion of CD4 cells, which results in impaired cellular immunity. During this early phase of infection, it is thought that the natural killer (NK) cells represent the main effector arm of the host immune response to HIV. This study investigates whether KIR and HLA factors are associated to CD4 T cell numbers after HIV infection in Mexican mestizos as assessed at the time of initial medical evaluation and subsequent clinical follow-up. KIR and HLA-B gene carrier frequency differences were compared between groups of patients stratified by CD4 T cell numbers as assessed during their first medical evaluation (a point in time at which all patients were anti-retroviral therapy naïve). In addition, the influence that these genetic factors have on averaged historical CD4 cell counts in patients subjected to follow-up (mostly therapy-experienced) was also evaluated. Our results suggest a protective role for the HLA-Bw4 and KIR3D + Bw4 combination in both therapy-naïve and therapy-experienced patients. This report furthers our understanding on the way that immune genes modulate HIV disease progression in less-studied human populations such as the Mexican mestizos with a special focus on CD4 T cell number and behaviour. [ABSTRACT FROM AUTHOR]

The article discusses a study of metastatic melanoma (MMEL) and metastatic renal cell carcinoma (MRCC) patients undergoing Interleukin -2 (IL-2) therapy to determine the correlation between T cell subset distribution and IL-2 therapy success. Topics include the use of flow cytometry to evaluate patient immune profiles, the comparison of changes in the distribution and phenotype of circulating CD4 and CD8 lymphocyte subsets, and treatment impact on effector lymphocytes and T cells.

Gold or mercury salts trigger a dramatic IgE response and a CD4 T-cell-dependent nephropathy in Brown-Norway (BN), but not in Lewis (LEW) rats. We previously identified the 1.1-Mb Iresp3 (immunoglobin response QTL3) locus on chromosome 9 that controls these gold salt-triggered immune disorders. In the present work, we investigated the genetic control of HgCl2-induced immunological disorders and assessed the relative contribution of the CD45RChigh and CD45RClow CD4 T-cell subpopulations in this control. By using interval-specific congenic lines, we narrowed down Iresp3 locus to 117-kb and showed that BN rats congenic for the LEW 117-kb were protected from HgCl2-triggered IgE response and nephropathy. This 117-kb interval also controls CD45RC expression by CD4 T cells and the ability of CD45RChigh CD4 T cells to trigger the autoimmune disorders resulting from HgCl2 administration. This 117-kb region contains four genes, including Vav1, a strong candidate gene according to its cellular function and exclusive expression in hematopoietic cells. Thus, this study highlights the role of the CD45RChigh CD4 T-cell subpopulation in the opposite susceptibility of BN and LEW rats to HgCl2-triggered immune disorders and identifies a 117-kb interval on chromosome 9 that has a key role in their functions. [ABSTRACT FROM AUTHOR]