title: Human neurocysticercosis: in vivo expansion of peripheral regulatory T cells and their recruitment in the central nervous system.
abstract: Human neurocysticercosis (NC) is caused by Taenia solium larvae lodged in the central nervous system. Most cases occur with no, or mild, neurological symptoms. However, in some patients, neuroinflammation is exacerbated, leading to severe forms of the disease. Considering the critical role of regulatory T cells (Tregs) in balancing inflammation in chronic diseases, their participation in restraining the inflammatory response in NC was explored in the present study. The frequency of Tregs and their relationship with the level of the proliferative response, the level of activated lymphocytes, and the cytokines expressed were determined in severe NC patients compared with those from healthy donors. Significantly increased peripheral Tregs (CD4(+)CD25(high) and CD4(+)CD25(high)FoxP3(+), CD4(+)CD25(high)CTLA4(+), and CD4(+)CD25(high) IL10(+)) and a significant decrease in activated (CD38(+) and CD69(+)) T cells were observed in 19 NC patients versus 10 healthy subjects. Significantly increased Tregs in NC are accompanied by a depressed specific, and non-specific, lymphocyte proliferative response, and they negatively correlate with activated CD4(+)CD69(+) lymphocytes. Treg frequencies were also determined in cerebral spinal fluid for 8 of the 19 NC patients. A positive significant correlation between peripheral and local Tregs was observed. Here, we report for the first time data that support the possible contribution of local and systemic Tregs in limiting neuroinflammation in NC.
authors.affiliation: Instituto Nacional de Neurología y Neurocirugía, Insurgentes Sur 3877, Col. La Fama, México DF, México.
authors.forename: Laura
authors.initials: L
authors.lastname: Adalid-Peralta
authors.forename: Agnes
authors.initials: A
authors.lastname: Fleury
authors.forename: Teresa M
authors.initials: TM
authors.lastname: García-Ibarra
authors.forename: Marisela
authors.initials: M
authors.lastname: Hernández
authors.forename: Michael
authors.initials: M
authors.lastname: Parkhouse
authors.forename: José Carlos
authors.initials: JC
authors.lastname: Crispín
authors.forename: Jefferson
authors.initials: J
authors.lastname: Voltaire-Proaño
authors.forename: Graciela
authors.initials: G
authors.lastname: Cárdenas
authors.forename: Gladis
authors.initials: G
authors.lastname: Fragoso
authors.forename: Edda
authors.initials: E
authors.lastname: Sciutto
mesh_terms: D000305:Adrenal Cortex Hormones / Q000008:administration & dosage; D000328:Adult; D000818:Animals; D016516:CD4-CD8 Ratio; D002490:Central Nervous System / Q000276:immunology*; D002555:Cerebrospinal Fluid / Q000166:cytology / Q000276:immunology; D003552:Cysticercus / Q000276:immunology; D016207:Cytokines / Q000097:blood / Q000134:cerebrospinal fluid; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D008213:Lymphocyte Activation; D008297:Male; D020019:Neurocysticercosis / Q000097:blood / Q000134:cerebrospinal fluid / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D041201:Taenia solium / Q000276:immunology; D014660:Vasoactive Intestinal Peptide / Q000097:blood / Q000134:cerebrospinal fluid
chemical_list: D000305:Adrenal Cortex Hormones; D016207:Cytokines; D053645:Interleukin-2 Receptor alpha Subunit; D014660:Vasoactive Intestinal Peptide