Interleukin-1? expression in capillaries and major histocompatibility complex class I expression in type II muscle fibers from polymyositis and dermatomyositis patients: Important pathogenic features independent of inflammatory cell clusters in muscle tissue

2002 ◽  
Vol 46 (4) ◽  
pp. 1044-1055 ◽  
Author(s):  
Pernilla Englund ◽  
Inger Nennesmo ◽  
Lars Klareskog ◽  
Ingrid E. Lundberg
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Muscle Tissue ◽  
Inflammatory Cell ◽  
Interleukin 1 ◽  
Class I ◽  
Type Ii ◽  
Complex Class ◽  
Cell Clusters ◽  
Histocompatibility Complex

scholarly journals NLRP3 Inflammasome Up-Regulates Major Histocompatibility Complex Class I Expression and Promotes Inflammatory Infiltration in Polymyositis

2021 ◽  
Author(s):  
Ping Xia ◽  
Yu-Quan Shao ◽  
Cong-Cong Yu ◽  
Yu Xie ◽  
Zhi-Jie Zhou
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Muscle Tissue ◽  
Nlrp3 Inflammasome ◽  
C2c12 Cells ◽  
Class I ◽  
Complex Class ◽  
Mhc I ◽  
Caspase 1 ◽  
Histocompatibility Complex

Abstract Backgrounds: This study was designed to investigate the role of the nucleotide-binding-domain (NBD)-and leucine-rich repeat (LRR)-containing (NLR) family, pyrin-domain-containing 3 (NLRP3) inflammasome in the pathogenesis of polymyositis (PM). Results: We found that the percentage of CD68+ cells, and the expression levels of NLRP3, caspase-1 and interleukin-1 beta (IL-1β) in the muscle tissue were elevated in 27 PM patients. LPS/ATP treatment in the Raw 264.7 macrophages resulted in activation of NLRP3 inflammasome and secretion of IL-1β as well as interferons (IFNs) and monocyte chemotactic protein-1 (MCP-1). Meanwhile, LPS/ATP challenged activation of NLRP3 inflammasome induced overexpression of major histocompatibility complex class I (MHC-I), a key molecular to develop to PM, in the co-cultured C2C12 cells. Genetic knockdown of NLRP3 inflammasome using siRNA or pharmacological inhibition of NLRP3 inflammasome using MCC950 effectively suppressed MHC-I overexpression in the co-cultured C2C12 cells. Certain levels of IL-1β rather than IFNs showed the effect of up-regulating MHC-I expression in C2C12 cells. IL-1β blockade using neutralizing IL-1β monoclonal antibody or siRNA of IL-1β suppressed MHC-I overexpression. In vivo, NLRP3 inflammasome inhibition using MCC950 reduced the expression of NLRP3, IL-1β and MHC-I in the muscle tissue of PM modal rats. Also, it attenuated the intensity of muscle inflammation as well as the CRP, CK, and LDH levels in the serum. Conclusions: Collectively, these results suggested that NLRP3/caspase-1/IL-1β axis may play an important role in the development of PM. Inhibition of NLRP3 activation may hold promise in the treatment of PM.

scholarly journals Modes of Calreticulin Recruitment to the Major Histocompatibility Complex Class I Assembly Pathway

2009 ◽  
Vol 285 (7) ◽  
pp. 4520-4535 ◽  
Author(s):  
Natasha Del Cid ◽  
Elise Jeffery ◽  
Syed Monem Rizvi ◽  
Ericca Stamper ◽  
Larry Robert Peters ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Assembly Pathway
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