PMID- 32430566
OWN - NLM
STAT- MEDLINE
DCOM- 20200911
LR  - 20200911
IS  - 1435-1250 (Electronic)
IS  - 0340-1855 (Linking)
VI  - 79
IP  - 6
DP  - 2020 Aug
TI  - [Pathogenesis of large vessel vasculitides].
PG  - 505-515
LID - 10.1007/s00393-020-00809-z [doi]
AB  - Large vessel vasculitides comprise two distinct entities, giant cell arteritis 
      (GCA) and Takayasu arteritis (TAK). GCA is the most common vasculitis in central 
      Europe, becoming manifested at an age over 50 years. In contrast, the much rarer 
      TAK affects almost exclusively young adults and mostly women. Both vasculitides 
      are granulomatous arteritides affecting mainly the aorta and its major arterial 
      branches. GCA and TAK are associated with different major histocompatibility 
      complex genes. Infections possibly play a role in the initiation of large vessel 
      vasculitides. Activation of dendritic cells in the adventitia induces chemokine 
      and cytokine-mediated recruitment and maturation of T‑helper (Th)1 and Th17 cells 
      and macrophages producing cytokines, growth factors and matrix 
      metalloproteinases. In GCA, CD4+ T‑helper cells and macrophages are predominantly 
      found in the inflammatory infiltrate. In TAK, the infiltrate also contains 
      cytotoxic CD8+ T‑cells and gammadelta T‑cells. This could indicate different antigenic 
      triggers in GCA and TAK. Inflammatory infiltration with T‑cells and macrophages 
      and activation of myofibroblasts and smooth muscular cells induce vascular 
      remodeling with intimal hyperplasia and destruction of the media. Remodeling is 
      histologically characterized by progressive arterial wall fibrosis, vascular 
      stenosis and obstruction. In summary, GCA and TAK represent two different 
      entities with a distinct human leukocyte antigen (HLA) and potentially 
      etiopathogenetic background. Clinically, inflammation-related general symptoms 
      and signs of ischemia are encountered, accompanied by increased levels of 
      serological markers of inflammation.
FAU - Arnold, S
AU  - Arnold S
AD  - Klinik fur Rheumatologie und klinische Immunologie, Universitat zu Lubeck, 
      Ratzeburger Allee 160, 23538, Lubeck, Deutschland.
FAU - Holl Ulrich, K
AU  - Holl Ulrich K
AD  - Pathologie - Hamburg, Labor Lademannbogen MVZ GmbH, Hamburg, Deutschland.
FAU - Lamprecht, P
AU  - Lamprecht P
AD  - Klinik fur Rheumatologie und klinische Immunologie, Universitat zu Lubeck, 
      Ratzeburger Allee 160, 23538, Lubeck, Deutschland. peter.lamprecht@uksh.de.
LA  - ger
PT  - Journal Article
PT  - Review
TT  - Pathogenese der Grossgefassvaskulitiden.
PL  - Germany
TA  - Z Rheumatol
JT  - Zeitschrift fur Rheumatologie
JID - 0414162
RN  - 0 (Cytokines)
SB  - IM
MH  - Adult
MH  - Cytokines
MH  - Europe
MH  - Female
MH  - *Giant Cell Arteritis/immunology/pathology
MH  - Humans
MH  - Macrophages
MH  - Male
MH  - *Takayasu Arteritis/immunology/pathology
MH  - Young Adult
OTO - NOTNLM
OT  - Giant cell arteritis
OT  - Granulomatous arteritis
OT  - Infections
OT  - Inflammation
OT  - Takayasu arteritis
EDAT- 2020/05/21 06:00
MHDA- 2020/09/12 06:00
CRDT- 2020/05/21 06:00
PHST- 2020/05/21 06:00 [pubmed]
PHST- 2020/09/12 06:00 [medline]
PHST- 2020/05/21 06:00 [entrez]
AID - 10.1007/s00393-020-00809-z [pii]
AID - 10.1007/s00393-020-00809-z [doi]
PST - ppublish
SO  - Z Rheumatol. 2020 Aug;79(6):505-515. doi: 10.1007/s00393-020-00809-z.