Blocking LFA-1 Aggravates Cardiac Inflammation in Experimental Autoimmune Myocarditis

Autor:	Stefan Brunner, Gabriela Kania, Valentina Seitelberger, Bruno C. Huber, Ludwig T. Weckbach, A. Uhl, Felicitas Boehm, Ulrich Grabmaier
Přispěvatelé:	University of Zurich
Rok vydání:	2019
Předmět:	CD4-Positive T-Lymphocytes Male 0301 basic medicine Neutrophils Lymphocyte Monocytes Nervous System Autoimmune Disease Experimental Mice 0302 clinical medicine Leukocyte Trafficking Medicine AC133 Antigen lcsh:QH301-705.5 Mice Inbred BALB C CD11b Antigen biology Stem Cells Communication 10051 Rheumatology Clinic and Institute of Physical Medicine Organ Size General Medicine Flow Cytometry Lymphocyte Function-Associated Antigen-1 Anti-Bacterial Agents medicine.anatomical_structure Integrin alpha M medicine.symptom Infiltration (medical) Myocarditis leukocytes T cell 610 Medicine & health Inflammation Autoimmune Diseases 03 medical and health sciences Antigen Leukemic Infiltration Animals business.industry Macrophages Body Weight medicine.disease 030104 developmental biology lcsh:Biology (General) Immunology biology.protein myocarditis business 030215 immunology
Zdroj:	Cells Cells, Vol 8, Iss 10, p 1267 (2019)
ISSN:	2073-4409
DOI:	10.3390/cells8101267
Popis:	The lymphocyte function-associated antigen 1 (LFA-1) is a member of the beta2-integrin family and plays a pivotal role for T cell activation and leukocyte trafficking under inflammatory conditions. Blocking LFA-1 has reduced or aggravated inflammation depending on the inflammation model. To investigate the effect of LFA-1 in myocarditis, mice with experimental autoimmune myocarditis (EAM) were treated with a function blocking anti-LFA-1 antibody from day 1 of disease until day 21, the peak of inflammation. Cardiac inflammation was evaluated by measuring infiltration of leukocytes into the inflamed cardiac tissue using histology and flow cytometry and was assessed by analysis of the heart weight/body weight ratio. LFA-1 antibody treatment severely enhanced leukocyte infiltration, in particular infiltration of CD11b+ monocytes, F4/80+ macrophages, CD4+ T cells, Ly6G+ neutrophils, and CD133+ progenitor cells at peak of inflammation which was accompanied by an increased heart weight/body weight ratio. Thus, blocking LFA-1 starting at the time of immunization severely aggravated acute cardiac inflammation in the EAM model.
Databáze:	OpenAIRE
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