PMID- 12791081
OWN - NLM
STAT- MEDLINE
DCOM- 20040310
LR  - 20201208
IS  - 0958-7578 (Print)
IS  - 0958-7578 (Linking)
VI  - 13
IP  - 3
DP  - 2003 Jun
TI  - Possible mechanisms underlying development of transfusion-related acute lung 
      injury: roles of anti-major histocompatibility complex class II DR antibody.
PG  - 141-7
AB  - Anti-major histocompatibility complex (anti-MHC) antibodies (Abs) and 
      antipolymorphonuclear neutrophil (anti-PMN) Abs are generally considered as the 
      main causes of the development of transfusion-related acute lung injury (TRALI), 
      which is one of the most severe and sometimes lethal side effects of transfusion. 
      These Abs are postulated to activate recipient's leucocytes, resulting in the 
      release of soluble factors such as reactive oxygen species and detrimental 
      cytokines and chemokines. The harmful effects on the lung tissues and resident 
      leucocytes of these malignant factors are suspected to be profoundly involved in 
      TRALI reactions. Several reports have indicated the principle effect of 
      biologically active lipids on the pathogenesis of TRALI. However, the precise 
      mechanisms of TRALI development remain unclear. To resolve this issue, we have 
      been investigating cytokines that induce continuous inflammation of the lungs, 
      specifically focusing on the cytokines derived from activated PMNs. We observed 
      that the granulocyte-macrophage colony-stimulating factor (GM-CSF) markedly 
      enhances the expression of MHC class II DR in PMNs. Moreover, MHC class II 
      DR-expressing PMNs were also proved to express a high-affinity receptor for 
      immunoglobulin E (IgE) (FcepsilonRI) and to produce tumour necrosis factor-alpha, 
      interferon-gamma and interleukin-18 following a challenge with an anti-MHC class 
      II DR monoclonal Ab (MoAb) or anti-DR antiserum. It is strongly suggested that 
      amongst various inflammatory mediators, at least these three cytokines may 
      contribute to the duration of inflammatory reactions in the lungs. Furthermore, 
      FcepsilonRI expression, in GM-CSF-treated PMNs, suggests the involvement of PMNs 
      in IgE-mediated immune reactions.
FAU - Nishimura, M
AU  - Nishimura M
AD  - Department of Research, Tokyo Metropolitan Red Cross Blood Center, Tokyo, Japan. 
      mo-nishimura@tokyo.bc.jrc.or.jp
FAU - Mitsunaga, S
AU  - Mitsunaga S
FAU - Ishikawa, Y
AU  - Ishikawa Y
FAU - Satake, M
AU  - Satake M
LA  - eng
PT  - Journal Article
PL  - England
TA  - Transfus Med
JT  - Transfusion medicine (Oxford, England)
JID - 9301182
RN  - 0 (Cytokines)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Isoantibodies)
RN  - 0 (Receptors, IgE)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Cytokines/biosynthesis
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology
MH  - HLA-DR Antigens/analysis/biosynthesis/*immunology
MH  - Humans
MH  - Inflammation/etiology
MH  - Isoantibodies/*immunology/pharmacology
MH  - Neutrophil Activation/immunology
MH  - Receptors, IgE/biosynthesis
MH  - Respiratory Distress Syndrome/etiology/*immunology
MH  - *Transfusion Reaction
MH  - Up-Regulation/drug effects
EDAT- 2003/06/07 05:00
MHDA- 2004/03/11 05:00
CRDT- 2003/06/07 05:00
PHST- 2003/06/07 05:00 [pubmed]
PHST- 2004/03/11 05:00 [medline]
PHST- 2003/06/07 05:00 [entrez]
AID - 434 [pii]
AID - 10.1046/j.1365-3148.2003.00434.x [doi]
PST - ppublish
SO  - Transfus Med. 2003 Jun;13(3):141-7. doi: 10.1046/j.1365-3148.2003.00434.x.