PMID- 32860200
OWN - NLM
STAT- MEDLINE
DCOM- 20210614
LR  - 20210614
IS  - 1179-1888 (Electronic)
IS  - 1175-0561 (Linking)
VI  - 21
IP  - 6
DP  - 2020 Dec
TI  - Novel Therapies for Pemphigus Vulgaris.
PG  - 765-782
LID - 10.1007/s40257-020-00544-w [doi]
AB  - Pemphigus vulgaris (PV) is a severe chronic autoimmune blistering disease that 
      affects the skin and mucous membranes. It is characterized by suprabasal 
      acantholysis due to disruption of desmosomal connections between keratinocytes. 
      Autoantibodies against desmosomal cadherins, desmoglein 3 and 1, have been shown 
      to induce disease. Certain human leukocyte antigen (HLA) types and non-HLA foci 
      confer genetic susceptibility. Until the discovery of corticosteroids in the 
      1950s, PV was 75% fatal. Since then, multiple PV treatments, such as systemic 
      corticosteroids and adjunctive therapy with immunosuppressive medications 
      (mycophenolate mofetil, azathioprine, cyclophosphamide, cyclosporine, 
      methotrexate, gold, and others) have been introduced; however, none have led to 
      long-term remissions and many have undesired adverse effects. Our growing 
      understanding of the pathophysiologic mechanisms in PV is leading to development 
      of new targeted therapies, such as intravenous immunoglobulin, anti-CD20 
      monoclonal antibodies, inhibitors of Bruton tyrosine kinase and neonatal Fc 
      receptors, and adoptive cellular transfer, that may result in lasting control of 
      this life-threatening disease.
FAU - Altman, Emily M
AU  - Altman EM
AUID- ORCID: 0000-0002-9768-8854
AD  - Department of Dermatology, University of New Mexico, 1021 Medical Arts Avenue NE, 
      Albuquerque, NM, 87102, USA. ealtman@salud.unm.edu.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - New Zealand
TA  - Am J Clin Dermatol
JT  - American journal of clinical dermatology
JID - 100895290
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antigens, CD20)
RN  - 0 (Autoantibodies)
RN  - 0 (HLA Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Receptors, Fc)
RN  - EC 2.7.10.2 (Agammaglobulinaemia Tyrosine Kinase)
RN  - EC 2.7.10.2 (BTK protein, human)
RN  - TW3XAW0RCY (Fc receptor, neonatal)
SB  - IM
MH  - Agammaglobulinaemia Tyrosine Kinase/antagonists & inhibitors/metabolism
MH  - Antibodies, Monoclonal/pharmacology/therapeutic use
MH  - Antigens, CD20/immunology/metabolism
MH  - Autoantibodies/immunology/metabolism
MH  - Combined Modality Therapy/methods
MH  - Drug Therapy, Combination/methods
MH  - Genetic Predisposition to Disease
MH  - HLA Antigens/genetics/immunology
MH  - Histocompatibility Antigens Class I/metabolism
MH  - Humans
MH  - Immunoglobulins, Intravenous/pharmacology/therapeutic use
MH  - Immunosuppressive Agents/pharmacology/*therapeutic use
MH  - Immunotherapy, Adoptive/*methods
MH  - Molecular Targeted Therapy/methods
MH  - Pemphigus/genetics/immunology/*therapy
MH  - *Plasmapheresis
MH  - Receptors, Fc/antagonists & inhibitors/metabolism
MH  - Remission Induction/methods
MH  - Signal Transduction/drug effects/immunology
MH  - Treatment Outcome
EDAT- 2020/08/30 06:00
MHDA- 2021/06/16 06:00
CRDT- 2020/08/30 06:00
PHST- 2020/08/30 06:00 [pubmed]
PHST- 2021/06/16 06:00 [medline]
PHST- 2020/08/30 06:00 [entrez]
AID - 10.1007/s40257-020-00544-w [pii]
AID - 10.1007/s40257-020-00544-w [doi]
PST - ppublish
SO  - Am J Clin Dermatol. 2020 Dec;21(6):765-782. doi: 10.1007/s40257-020-00544-w.