scholarly journals Overview on Diagnosis and Management of Polymyositis

2021 ◽  
pp. 445-451
Author(s):  
Mohammed Salah Hussein ◽  
Atyaf Khalid Almandeil ◽  
Sarah Shujaa Alsulami ◽  
Amaal Abdulrahman Alwayli ◽  
Amal Abdulrahman Alwayli ◽  
...  
Keyword(s):  
Cytotoxic T Lymphocytes ◽  
Skeletal Muscles ◽  
Inclusion Body Myositis ◽  
Autoimmune Disorder ◽  
Complex Class ◽  
Older Individuals ◽  
Cd8 Cells ◽  
Histocompatibility Complex ◽  
Class 1 ◽  
Residual Muscle Weakness

Polymyositis (PM) is an autoimmune disorder; result from abnormal activation of cytotoxic T lymphocytes (CD8 cells) and macrophages against muscular antigens as well as the strong extrafusal muscular expression of major histocompatibility complex class 1 causing damage to the endomysium of the skeletal muscles.  Polymyositis develops over the months as compared to inclusion body myositis (IBM), which is a slowly progressive chronic myopathy developing in older individuals over a period of months to years with more severe symptoms.  Many patients require treatment for many years. Polymyositis affects the distal musculature of the esophagus in the late stage of disease in up to 70% of the patients leading to the inability to swallow, as well as regurgitation problems that can cause aspiration pneumonia. The principal goals of therapy are to improve strength and improve physical functioning. Many patients require treatment for several years. The 5-year survival rate for treated patients is in the order of 95%. Up to one-third of PM patients may be left with some degree of residual muscle weakness.

Clinicopathologic features of myositis patients with CD8-MHC-1 complex pathology

Neurology ◽  
2017 ◽  
Vol 89 (10) ◽  
pp. 1060-1068 ◽  
Author(s):  
Chiseko Ikenaga ◽  
Akatsuki Kubota ◽  
Masato Kadoya ◽  
Kenichiro Taira ◽  
Naohiro Uchio ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Inclusion Body Myositis ◽  
Muscle Fibers ◽  
Immunosuppressive Treatment ◽  
Complex Class ◽  
Clinicopathologic Features ◽  
Hepatitis C Virus Infection ◽  
Histocompatibility Complex ◽  
Histopathologic Finding ◽  
Class 1

Objective:To determine the clinical features of myositis patients with the histopathologic finding of CD8-positive T cells invading non-necrotic muscle fibers expressing major histocompatibility complex class 1 (CD8-MHC-1 complex), which is shared by polymyositis (PM) and inclusion body myositis (IBM), in relation to the p62 immunostaining pattern of muscle fibers.Methods:All 93 myositis patients with CD8-MHC-1 complex who were referred to our hospital from 1993 to 2015 were classified on the basis of the European Neuromuscular Center (ENMC) diagnostic criteria for IBM (Rose, 2013) or PM (Hoogendijk, 2004) and analyzed.Results:The 93 patients included were 17 patients with PM, 70 patients with IBM, and 6 patients who neither met the criteria for PM nor IBM in terms of muscle weakness distribution (unclassifiable group). For these PM, IBM, and unclassifiable patients, their mean ages at diagnosis were 63, 70, and 64 years; autoimmune disease was present in 7 (41%), 13 (19%), and 4 (67%); hepatitis C virus infection was detected in 0%, 13 (20%), and 2 (33%); and p62 was immunopositive in 0%, 66 (94%), and 2 (33%), respectively. Of the treated patients, 11 of 16 PM patients and 4 of 6 p62-immunonegative patients in the unclassifiable group showed responses to immunotherapy, whereas all 44 patients with IBM and 2 p62-immunopositive patients in the unclassifiable group were unresponsive to immunotherapy.Conclusions:CD8-MHC-1 complex is present in patients with PM, IBM, or unclassifiable group. The data may serve as an argument for a trial of immunosuppressive treatment in p62-immunonegative patients with unclassifiable myositis.

scholarly journals A Human Herpesvirus 7 Glycoprotein, U21, Diverts Major Histocompatibility Complex Class I Molecules to Lysosomes

2001 ◽  
Vol 75 (24) ◽  
pp. 12347-12358 ◽  
Author(s):  
Amy W. Hudson ◽  
Peter M. Howley ◽  
Hidde L. Ploegh
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Cytotoxic T Lymphocytes ◽  
Human Herpesvirus ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Infected Cells ◽  
Immune Detection

ABSTRACT All members of the herpesvirus family persist in their host throughout life. In doing so, herpesviruses exploit a surprising number of different strategies to evade the immune system. Human herpesvirus 7 (HHV-7) is a relatively recently discovered member of the herpesvirus family, and little is known about how it escapes immune detection. Here we show that HHV-7 infection results in premature degradation of major histocompatibility complex class I molecules. We identify and characterize a protein from HHV-7, U21, that binds to and diverts properly folded class I molecules to a lysosomal compartment. Thus, U21 is likely to function in the normal course of HHV-7 infection to downregulate surface class I molecules and prevent recognition of infected cells by cytotoxic T lymphocytes.

scholarly journals Two Major Histocompatibility Complex Class I-Restricted Epitopes of the Borna Disease Virus p10 Protein Identified by Cytotoxic T Lymphocytes Induced by DNA-Based Immunization

2003 ◽  
Vol 77 (10) ◽  
pp. 6076-6081 ◽  
Author(s):  
Yoshio Hashimoto ◽  
Horng-Shen Chen ◽  
Cynthia Cunningham ◽  
Tahir H. Malik ◽  
Patrick K. Lai
Keyword(s):  
Major Histocompatibility Complex ◽  
T Lymphocytes ◽  
Antibody Response ◽  
Major Histocompatibility Complex Class ◽  
Disease Virus ◽  
Cytotoxic T Lymphocytes ◽  
Complex Class ◽  
Lewis Rats ◽  
Histocompatibility Complex ◽  
Borna Disease

ABSTRACT Borna disease virus (BDV) infection of Lewis rats is the most studied animal model of Borna disease, an often fatal encephalomyelitis. In this experimental model, BDV-specific CD8+ cytotoxic T lymphocytes (CTLs) play a prominent role in the immunopathogenesis of infection by the noncytolytic, persistent BDV. Of the six open reading frames of BDV, CTLs to BDV X (p10) and the l-polymerase have never been studied. In this study, we used plasmid immunization to investigate the CTL response to BDV X and N. Plasmid-based immunization was a potent CTL inducer in Lewis rats. Anti-X CTLs were primed by a single injection of the p10 cDNA. Two codominant p10 epitopes, M1SSDLRLTLL10 and T8LLELVRRL16, associated with the RT1.Al major histocompatibility complex class I molecules of the Lewis rats, were identified. In addition, immunization with a BDV p40-expressing plasmid confirmed the previously reported RT1.Al-restricted A230SYAQMTTY238 peptide as the CTL target for BDV N. In contrast to the CTL responses, plasmid vaccination was a poor inducer of an antibody response to p10. Three injections of a recombinant eukaryotic expression plasmid of BDV p10 were needed to generate a weak anti-p10 immunoglobulin M response. However, the antibody response could be optimized by a protein boost after priming with cDNA.

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