ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02099.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02100.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Molecular biology has made the transition from phase 1, dealing with prokaryotic genes and DNA, to phase 2, dealing with genes of eukaryotic multicellular organisms. This transition came about because of the DNA technology that has evolved since the early 1970s. Now we are at the beginning of the transition to phase 3, through the emerging human genome project. The background of the development of this project, its current state, and its possible impact on the life sciences is briefly outlined and discussed.

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02101.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02102.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02103.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02104.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02105.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02106.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02107.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Recent studies of the cellular mechanisms involved in chronic inflammatory periodontal disease (CIPD) have contributed significantly to our understanding of the pathogenesis of the disease process. Functional studies have demonstrated polymorphonuclear neutrophil (PMN) chemotactic defects in some 70% of subjects with localized juvenile periodontitis while chemiluminescence data have suggested that periphertal blood PMNs from young subjects with adult periodontitis (AP) may be in a metabolically active state. Further studies have shown that stimulation of PMNs with a number of periodontopathic bacteria resulted in the production of an IL‐1 inhibitor suggesting a possible regulatory role for PMNs in CIPD in addition to their established protective role. Most work on the immunoregulation of CIPD has, however, concentrated on T‐cells. Recent limit dilution analysis has demonstrated the presence of periodontopathic bacteria‐specific T cells in peripheral blood and the involvement and homing of these cells to the local lesions of CIPD is currently the focus of many studies. In animal studies,Actinobacillus actinomycetemcomitans (Aa)‐specific T‐cell clones home to the gingival tissues where they may exert a protective role. Homing and retention of lymphocytes to and in specific sites is dependent upon the expression of adhesion molecules. Recent data indicate however, that while there are increasing levels of ICAM‐1, LECAM‐1 and PECAM‐1 expression with increasing degrees of inflammation, there are no differences between gingivitis and periodontitis lesions. Cytokine profiles may be related to the role of T‐cell clones homing to the gingiva in CIPD. In subjects susceptible to periodontal breakdown there may be an increase in the type 2 IL‐4 producing T‐cells whereas in non‐susceptible subjects, type 1 IL‐2/IFN‐γ producing T‐cells may preferentially home to the gingiva. This hypothesis is generally supported by recent data obtained from human studies but data obtained from animal studies is only partly supportive and may suggest the opposite. Nevertheless, it is now possible to construct a testable framework or model of CIPD based on these cel

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1993.tb02108.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY