Efficacy of immunotherapy in obese patients with cancer.

Obesity is a condition of excessive fat tissue and high body mass index (BMI ≥30), which is increasing worldwide. Excess body weight is associated with poorer results in cancer treatments; however, recent studies emphasized that elevated BMI was associated with improved outcomes in cases treated by immune checkpoint inhibitor (ICI) therapies, which is called the obesity paradox. In this review, we discuss the correlation between obesity and cancer immunotherapy, especially ICIs, the underlying mechanisms, and the outcomes in different types of cancers. In addition, we describe the occurrence of immune-related adverse events and the effect of gender in obese patients during immunotherapy using all relevant studies with available full texts.

Rheumatoid Arthritis Susceptibility Is Associated with the KIR2DS4-Full of Killer-Cell Immunoglobulin-Like Receptor Genes in the Lur Population of Iran.

BACKGROUND: The pathophysiology underlying the progression and development of autoimmune conditions, such as Rheumatoid Arthritis (RA), is a result of dysregulations of the immune system. Research has explored the genetic alterations present in RA; however, limited studies have examined the role of Killer cell Immunoglobulin-like Receptors (KIR) and Human Leukocyte Antigen (HLA) molecules in RA. Therefore, the aim of this study was to examine KIR genes, their HLA ligands, and KIR-HLA compounds in patients with RA. METHODS: In this case-control study, a total of 50 patients with RA and 100 healthy individuals were enrolled. DNA samples were evaluated using PCR with sequence specific Primers (PCR-SSP). Odds ratio (OR) with a 95% confidence interval (CI) were reported. RESULTS: Among the KIR genes examined, KIR2DLA (p= 0.0255, OR= 0.389, 95% CI= 0.210-0.722) and KIR2DS4-full (p< 0.0001, OR= 6.163, 95% CI= 3.174-11.968) were observed to have a statistically significant correlation with disease susceptibility to RA. As an inhibitory gene, KIR2DLA was observed to have a protective effect against RA while KIR2DS4-full as an activating gene, was found to increase risk for RA. No significant associations were found between any of the other KIR genotypes, HLA ligands, or KIR-HLA compounds examined in this study to RA susceptibility. CONCLUSION: In this study of RA in the Lur population of Iran, KIR2DS4-full was observed to increase susceptibility to RA, while KIR2DL5A was found to act as a protecting factor based on both the cross Table and regression analyses. Further research should focus on repeating this study in additional populations.