title: Phenotypic changes in immune cell subsets reflect increased infarct volume in male vs. female mice.
abstract: Inflammatory responses in the brain after cerebral ischemia have been studied extensively in male mice, but not female mice, thus potentially giving a less-than-accurate view of gender associated pathological processes. In humans, cerebral infarcts are typically smaller in premenopausal females than in age-matched males. In the current study, we confirmed smaller infarcts in female vs. male mice after middle cerebral artery occlusion and 96 h of reperfusion. Moreover, we explored immunological alterations related to this difference and found that the percentage of CD4+ T lymphocytes was significantly higher in spleens in males than females, with increased expression of the activation markers, CD69 and CD44. In contrast, the percentage of CD8+ T lymphocytes was significantly higher in spleens of females than males, leading to the identification of a small but distinct population of IL-10-secreting CD8+CD122+ suppressor T cells that were also increased in females. Finally, we observed that males have a greater percentage of activated macrophages/microglia in the brain than females, as well as increased expression of the VLA-4 adhesion molecule in both brain and spleen. This new information suggesting gender-dependent immunological mechanisms in stroke implies that effective treatments for human stroke may also be gender specific.
authors.forename: Anirban
authors.initials: A
authors.lastname: Banerjee
authors.forename: Jianming
authors.initials: J
authors.lastname: Wang
authors.forename: Sheetal
authors.initials: S
authors.lastname: Bodhankar
authors.forename: Arthur A
authors.initials: AA
authors.lastname: Vandenbark
authors.forename: Stephanie J
authors.initials: SJ
authors.lastname: Murphy
authors.forename: Halina
authors.initials: H
authors.lastname: Offner
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000276:immunology / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D002544:Cerebral Infarction / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D018960:Hyaluronan Receptors / Q000276:immunology / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D039041:Integrin alpha4beta1 / Q000276:immunology / Q000378:metabolism; D016753:Interleukin-10 / Q000276:immunology / Q000378:metabolism; D053646:Interleukin-2 Receptor beta Subunit / Q000276:immunology / Q000378:metabolism; D037181:Lectins, C-Type / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D015427:Reperfusion Injury / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D012737:Sex Factors; D013154:Spleen / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D018960:Hyaluronan Receptors; D039041:Integrin alpha4beta1; D016753:Interleukin-10; D053646:Interleukin-2 Receptor beta Subunit; D037181:Lectins, C-Type; D000099192:CD69 Antigens