Ultraviolet B (UVB) irradiation interferes with the afferent and efferent loops of the immune response. One mechanism that has been suggested is the decline of class II histocompatibility antigen expression on the cell surface. However, data in the literature are controversial. In the present study, we examined the effect of UVB light (peak emission at 302 nm), at doses of 0.05-300 mJ/cm2, on class II antigen expression on normal peripheral blood lymphocytes enriched for non-T cells. Monoclonal antibodies directed at nonpolymorphic determinants on HLA-DR, -DQ, and -DP were used to label cells before and at time intervals up to 72 h after irradiation. Immediately following UVB exposure, fluorescence intensity for all three antigens was equal to or slightly increased above control values. Subsequently, there was a decline in antigen expression that was UVB dose dependent and varied for HLA-DR, -DP and -DQ. Although there was only a very moderate loss of surface labeling for HLA-DR up to 72 h, there was a steep decline for HLA-DQ and -DP. There was no significant decline in class II antigen expression on cells exposed to 2000 or 4000 cGy of gamma irradiation. Also, there was no effect of either gamma or UVB irradiation on class I antigen expression. These data explain some of the discrepancies in previous reports on the effects of UVB on class II antigens; they show not only a dose effect but also an effect of time after exposure and, most importantly, the class II antigen under study.
Download full-text PDF |
Source |
---|
Blood Adv
January 2025
The University of Sydney, Sydney, Australia.
T-cell receptor (TCR) therapies are a promising modality for the treatment of cancers, with significant efforts being directed towards acute myeloid leukaemia (AML), a particularly challenging disease. Chimeric antigen receptor (CAR) T-cells targeting single surface antigens have shown remarkable efficacy for B-cell lymphoblastic leukaemia, lymphomas and multiple myeloma. However, AML presents formidable obstacles to the effectiveness of CAR T-cells due to the widespread expression of heterogenous leukaemia immunophenotypes and surface antigen targets additionally present on normal myeloid cells.
View Article and Find Full Text PDFProtein Cell
January 2025
State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory, School of Public Health, Xiamen University, Xiamen 361102, China.
Antibody-drug conjugates (ADCs) represent a promising class of targeted cancer therapeutics that combine the specificity of monoclonal antibodies with the potency of cytotoxic payloads. Despite their therapeutic potential, the use of ADCs faces significant challenges, including off/on-target toxicity and resistance development. This review examines the current landscape of ADC development, focusing on the critical aspects of target selection and antibody engineering.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Faculty of Applied Sciences & Biotechnology, Shoolini University, Solan, 173229, India.
Background: The role and relevance of macrophages both as causes and therapeutics of cellular senescence is rapidly emerging. However, current knowledge regarding the extent and depth of senescence in macrophages in vivo is limited and controversial. Further, acute models of stress-induced senescence in transformed/cancerous macrophage cell lines are being used although their efficacy and relevance are not characterized.
View Article and Find Full Text PDFComb Chem High Throughput Screen
January 2025
Thoracic and Abdominal Radiotherapy Department I, Meizhou People's Hospital, Meizhou 514031, Guangdong, China.
Background: TSPOAP1 antisense RNA 1 (TSPOAP1-AS1) is a long non-coding RNA (lncRNA) that has received widespread attention in oncology research in recent years. Its role and mechanism in some cancers have gradually been revealed. However, it is not clear what role TSPOAP1-AS1 plays in cervical cancer (CESC).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!