The two primary forms of inflammatory disorders of the small intestine andcolon that make up inflammatory bowel disease (IBD) are ulcerative colitis (UC) and Crohn\'s disease (CD). While ulcerative colitis primarily affects the colon and the rectum, CD affects the small and large intestines, as well as the esophagus,mouth, anus, andstomach. Although the etiology of IBD is not completely clear, and there are many unknowns about it, the development, progression, and recurrence of IBD are significantly influenced by the activity of immune system cells, particularly lymphocytes, given that the disease is primarily caused by the immune system stimulation and activation against gastrointestinal (GI) tract components due to the inflammation caused by environmental factors such as viral or bacterial infections, etc. in genetically predisposed individuals. Maintaining homeostasis and the integrity of the mucosal barrier are critical in stopping the development of IBD. Specific immune system cells and the quantity of secretory mucus and microbiome are vital in maintaining this stability. Th22 cells are helper T lymphocyte subtypes that are particularly important for maintaining the integrity and equilibrium of the mucosal barrier. This review discusses the most recent research on these cells\' biology, function, and evolution and their involvement in IBD.

Atherosclerosis and its complications are a major cause of morbidity and mortality worldwide in spite of the improved medical and invasive treatment in terms of revascularization. Atherosclerosis is a dynamic, multi-step process in which inflammation is a ubiquitous component participating in the initiation, development, and entanglements of the atherosclerotic plaque. After activation, the immune system, either native or acquired, is part of the atherosclerotic dynamics enhancing the pro-atherogenic function of immune or non-immune cells, such as endothelial cells, smooth muscle cells, or platelets, through mediators such as cytokines or directly by cell-to-cell interaction. Cytokines are molecules secreted by the activated cells mentioned above that mediate the inflammatory component of atherosclerosis whose function is to stimulate the immune cells and the production of further cytokines. This review provides insights of the cell axis activation and specific mechanisms and pathways through which inflammation actuates atherosclerosis.

UNASSIGNED: According to the previous studies, general anesthesia influences the immune system. Evaluating such impacts on the immune system helps to improve the management of anesthesia.
UNASSIGNED: The current review aimed to summarize the literature related to the effects of general anesthesia agents on the cytokines. Google Scholar, PubMed, and ISI/Web of Sciences databases were searched using the following keywords: cytokine, general anesthesia, immune response, intravenous anesthetics, volatile anesthetics, opioids, benzodiazepines, and controlled ventilation.
UNASSIGNED: Long-term administration of general anesthesia drugs, due to their effects on cytokines, can lead to disease progression in patients with immune deficiency. Due to the conflicting results of various studies and the increasing number of patients with immune deficiency, the choice of the appropriate general anesthesia agents facilitates achieving the more favorable function of the cytokines.
UNASSIGNED: It seems that the effect of general anesthesia on the immune system in healthy patients and short-term surgeries is not considerable and changes in the immune system are related to surgical trauma, particularly in major surgery.

Leptin is a regulatory hormone with multiple roles in the immune system. We favor the concept that leptin signaling \'licenses\' various immune cells to engage in immune responses and/or to differentiate. Leptin is an inflammatory molecule that is capable of activating both adaptive and innate immunity. It can also \'enhance\' immune functions, including inflammatory cytokine production in macrophages, granulocyte chemotaxis, and increased Th17 proliferation. Leptin can also \'inhibit\' cells; CD4(+) T cells are inhibited from differentiating into regulatory T cells in the presence of elevated leptin, while NK cells can exhibit impaired cytotoxicity under the same circumstances. Consequently, understanding the effect of leptin signaling is important to appreciate various aspects of immune dysregulation observed in malnutrition, obesity, and autoimmunity.