PMID- 9798188
OWN - NLM
STAT- MEDLINE
DCOM- 19990129
LR  - 20191102
IS  - 0927-3948 (Print)
IS  - 0927-3948 (Linking)
VI  - 6
IP  - 1
DP  - 1998 Mar
TI  - Role of inflammatory cytokines in induction of anterior chamber-associated immune 
      deviation.
PG  - 1-11
AB  - PURPOSE: To determine the extent to which proinflammatory cytokines 
      [(interleukin-I-beta (IL-1 beta), tumor necrosis factor-alpha (TNF alpha), 
      gamma-interferon (gamma-IFN)] interfere with induction of anterior 
      chamber-associated immune deviation (ACAID). METHODS: Proinflammatory cytokines 
      were injected intracamerally prior to local injection of ovalbumin (OVA), or 
      added to cultures containing peritoneal exudate cells (PEC), transforming growth 
      factor-beta (TGF beta), and OVA. After incubation, these cells were washed and 
      injected intravenously into naive, syngeneic mice. One week later, the mice were 
      immunized with OVA in adjuvant, and delayed hypersensitivity (DH) was assessed 
      seven days later. RESULTS: Eyes pretreated with IL-1 beta, TNF alpha or gamma-IFN 
      failed to support ACAID induction. In addition, IL-1 beta and gamma-IFN robbed 
      OVA-pulsed, TGF beta-treated PEC of their ability to induce ACAID, whether the 
      inflammatory cytokines were added prior to, simultaneously with, or after 
      exposure to TGF beta. By contrast, in-vitro exposure of PEC to TNF alpha was 
      unable to prevent TGF beta-promoted ACAID. CONCLUSION: IL-1 beta, gamma-IFN, and 
      TNF alpha injected intracamerally rob the eye of immune privilege and prevent 
      ACAID induction. In the cases of IL-1 beta and gamma-IFN, ACAID seems to be 
      prevented by a direct action of the cytokines on antigen-presenting cells (APCs). 
      In the case of TNF alpha, prevention of ACAID in vivo probably occurs by an 
      APC-independent mechanism.
FAU - Okamoto, S
AU  - Okamoto S
AD  - Department of Ophthalmology, Ehime University Medical School, Japan.
FAU - Streilein, J W
AU  - Streilein JW
LA  - eng
GR  - EY 05678/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Ocul Immunol Inflamm
JT  - Ocular immunology and inflammation
JID - 9312169
RN  - 0 (Interleukin-1)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Animals
MH  - Anterior Chamber/*immunology
MH  - Antigen-Presenting Cells/physiology
MH  - Exudates and Transudates/cytology
MH  - Hypersensitivity, Delayed/immunology/physiopathology/*prevention & control
MH  - Interferon-gamma/*pharmacology
MH  - Interleukin-1/*pharmacology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Ovalbumin/immunology
MH  - Peritoneal Cavity/cytology
MH  - Transforming Growth Factor beta/immunology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1998/11/03 00:00
MHDA- 1998/11/03 00:01
CRDT- 1998/11/03 00:00
PHST- 1998/11/03 00:00 [pubmed]
PHST- 1998/11/03 00:01 [medline]
PHST- 1998/11/03 00:00 [entrez]
AID - 10.1076/ocii.6.1.1.8081 [doi]
PST - ppublish
SO  - Ocul Immunol Inflamm. 1998 Mar;6(1):1-11. doi: 10.1076/ocii.6.1.1.8081.