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1

Genetic aspects of atopic disorders

100%
Rymarczyk B., Rogala R.
Postępy Higieny i Medycyny Doświadczalnej
|
2000
|
vol. 54
|
issue 5
657-667
EN
Atopy tends to run in families, suggesting the existene of a genetic predisposition. This review contains actual knowledge of the genetic basis of atopic disorders.
2

Bronchial asthma as a multifactorial disease

80%
Jasek M.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 3
263-273
EN
Asthma is a common condition that results from the interaction of an unknown number of genes with envitonmental factors. Here, we describe the recent advances in this field including results of genome-wide searches for susceptibility genes.
3

Pathogenetic mechanisms of atopic dermatitis

70%
Pastore S., Giustizieri M. L., Mascia F., Giannetti A., Girolomoni G.
Archivum Immunologiae et Therapiae Experimentalis
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2000
|
vol. 48
|
issue 5
497-504
EN
Atopic dermatitis (AD) is a chronic inflammatory disease which results from complex interactions between genetic and environmental mechanisms. An altered lipid composition of the stratum corneum is responsible of the xerotic aspect of the skin, and determines a higher permeability to allergens and irritants. Keratinocytes of AD patients exhibit a propensity to an exaggerated production of cytokines and chemokines, a phenomenon that can have a major role in promoting and maintaining inflammation. Specific immune responses against a variety of environmental allergens are also implicated in AD pathogenesis with a bias towards Th2 immune responses. In particular, dendritic cells expressing membrane IgE receptors, play a critical role in the amplification of allergen-specific T cell responses. Cross-linkage of specific IgE receptors on dermal mast cells provokes release and synthesis of a vast series of mediators. Following their recruitment and activation into the skin, eosinophils are also thought to contribute relevantly to tissue damage. Thus, a complex network of cytokines and chemokines contributes to establish a local milieu that favors the permanence of inflammation in AD skin.
4

A review of asthma genetics: gene expression studies and recent candidates

61%
Malerba G., Pignatti P. F.
Journal of Applied Genetics
|
2005
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vol. 46
|
issue 1
93-104
EN
Recent evidence indicates an important role of inflammation pathways, airways remodeling and epithelium activation in asthma genetics. In particular, transcriptome studies have detected differentially expressed genes involved in eosinophil apoptosis, the arginase pathway, response to allergens or interleukins, and to inhaled corticosteroids. Candidate gene and genome wide studies have localized genetic regions involved in the disease, such as the A1AR and CLCA1 genes (chromosome 1), IL-1RN and DPP10 (2q14), HLA-G and TNF- (6p21), GPRA (7p14), FcRI and GSTP1 (11q13), NOS1, IFNG, STAT6, VDR, and other genes (12q13-26), PHF11 and flanking genes (13q14), AACT and PTGDR (14q), and ADAM33 (20p13). The role of these and other genetic determinants has to be confirmed in future, preferably longitudinal, studies.
5

T cell chemokine receptor expression in human Th1- and Th2-associated diseases

61%
Campbell J. D., Hayglass K. T.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 5
451-456
EN
The interaction between chemokines and their receptors is an important step in the control of leukocyte migration into sites of inflammation. Chemokines also mediate a variety of effects independent of chemotaxis, including induction and enhancement of Th1- and Th2---associated cytokine responses. Recent studies have shown that human Th1 and Th2 clones, activated under polarizing conditions with polyclonal stimuli in vitro, display distinct patterns of chemokine receptor expression: Th1 clones preferentially express CCR5 and CXCR3 while many Th2 clones express CCR4, CCR8 and, to a lesser extent, CCR3. These differential patterns of chemokine receptor expression suggest a mechanism for selective induction of migration and activation of Th1- and Th2-type cells during inflammation and, perhaps, normal immune homoeostasis. Studies have begun to examine T cell chemokine receptor expression in vivo to determine the relevance of these in vitro observations to human Th1 and Th2-associated diseases. In this review, we critically examine recent reports of T cell chemokine receptor expression in human autoimmune disorders (multiple sclerosis and rheumatoid arthritis) and atopic disorders (allergic rhinitis and asthma) which are believed to arise from inappropriate Th1- and Th2-dominated responses, respectively.
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