PMID- 12930367
OWN - NLM
STAT- MEDLINE
DCOM- 20031014
LR  - 20190513
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 133
IP  - 3
DP  - 2003 Sep
TI  - Influence of human T lymphotrophic virus type I on cryptogenic fibrosing 
      alveolitis - HTLV-I associated fibrosing alveolitis: proposal of a new clinical 
      entity.
PG  - 397-403
AB  - Human T lymphotrophic virus type-I (HTLV-I), a human retrovirus, infects CD4+ 
      lymphocytes and is thought to modify their function; a possible association with 
      pulmonary diseases has also been suggested. However, little is known about the 
      influence of HTLV-I on cryptogenic fibrosing alveolitis (CFA), a chronic 
      inflammatory interstitial lung disease of unknown aetiology. In order to clarify 
      the influence of HTLV-I infection on CFA, 72 CFA patients with and without HTLV-I 
      infection were examined. HTLV-I positive CFA patients were likely to have larger 
      affected areas and to show traction bronchiectasis with honeycombing change. An 
      imbalance of matrix metalloproteinases and tissue inhibitor of metalloproteinases 
      were also observed in the BALF of HTLV-I positive CFA patients. CD3+/CD25+ 
      lymphocyte percentage was significantly higher in the BALF of HTLV-I positive 
      patients compared to negative patients. MIP-1alpha, IP-10 and sICAM levels in 
      BALF were also significantly higher in HTLV-I positive patients than in negative 
      patients. The levels of MCP-1 and IL-8 were not significantly different. In 
      HTLV-I positive patients, the MIP-1alpha and IP-10 levels showed a significant 
      positive correlation with percentage of CD3+/CD25 lymphocytes. HTLV-I positive 
      CFA patients showed a larger lesion than negative patients and exhibited 
      increased levels of certain cytokines that correlated with activated T cells in 
      the BALF. We suggest that HTLV-I infection may contribute to the development of 
      CFA via activation of T cells. We also propose that these features should be 
      taken into consideration in the treatment of CFA in HTLV-I infected individuals.
FAU - Matsuyama, W
AU  - Matsuyama W
AD  - Third Department of Internal Medicine, Kagoshima University Faculty of Medicine, 
      Kagoshima, Japan. vega@xa2.so-net.ne.jp
FAU - Kawabata, M
AU  - Kawabata M
FAU - Mizoguchi, A
AU  - Mizoguchi A
FAU - Iwami, F
AU  - Iwami F
FAU - Wakimoto, J
AU  - Wakimoto J
FAU - Osame, M
AU  - Osame M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (CD3 Complex)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (HTLV-I Antibodies)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Receptors, Interleukin-2)
RN  - 0 (Tissue Inhibitor of Metalloproteinases)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Analysis of Variance
MH  - Bronchoalveolar Lavage Fluid/chemistry
MH  - CD3 Complex/analysis
MH  - Case-Control Studies
MH  - Cell Adhesion Molecules/analysis
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Chemokine CXCL10
MH  - Chi-Square Distribution
MH  - HTLV-I Antibodies/blood
MH  - HTLV-I Infections/*complications/immunology/pathology
MH  - *Human T-lymphotropic virus 1
MH  - Humans
MH  - Lung/immunology/pathology
MH  - Lymphocyte Activation
MH  - Macrophage Inflammatory Proteins/analysis
MH  - Matrix Metalloproteinases/analysis
MH  - Middle Aged
MH  - Prevalence
MH  - Pulmonary Fibrosis/immunology/pathology/*virology
MH  - Receptors, Interleukin-2/analysis
MH  - Retrospective Studies
MH  - T-Lymphocytes/immunology
MH  - Tissue Inhibitor of Metalloproteinases/analysis
PMC - PMC1808791
EDAT- 2003/08/22 05:00
MHDA- 2003/10/15 05:00
PMCR- 2004/09/01
CRDT- 2003/08/22 05:00
PHST- 2003/08/22 05:00 [pubmed]
PHST- 2003/10/15 05:00 [medline]
PHST- 2003/08/22 05:00 [entrez]
PHST- 2004/09/01 00:00 [pmc-release]
AID - 2240 [pii]
AID - 10.1046/j.1365-2249.2003.02240.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2003 Sep;133(3):397-403. doi: 10.1046/j.1365-2249.2003.02240.x.