By S. Holgate, et. al.
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As the distance between the disease locus and a marker locus increases so the chance of recombination in the interval between them increases and the proportion of recombinant increases. If the disease and marker loci are separated by a considerable distance on the same chromosome, then crossover between the loci is highly likely and the disease and marker traits will occur separately in each recombinant but together in non-recombinants. The evidence for linkage of a genomic region to a phenotype of interest is usually expressed in terms of the ratio of their odds of the two hypotheses (linkage or nonlinkage), the likelihood ratio (LR), or more equivalently by the lod score (Z), where Z = log10(LR).
ICAM-1, intercellular adhesion molecule-1; MAdCAM-1, mucosal address in cell adhesion molecule-1; PECAM-1, platelet/endothelial cell adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1. inflammation. 4) target a variety of cell types important to allergic inflammation including eosinophils, basophils, lymphocytes, macrophages, and dendritic cells, whereas the CXC chemokines mainly target neutrophils and mononuclear cells. Stimuli that induce chemokine expression Many of the stimuli for secretion of chemokines are the early signals elicited during innate immune responses including proinflammatory cytokines (such as IL-1β and TNF-α), which are released at sites of allergic inflammation.
Clinical trials with cytokine antagonists, chemokine inhibitors, adhesion molecule antagonists, or compounds that interfere with intracellulalar signalling pathways or the transcription of genes important to allergic inflammation will improve our understanding of the function of these individual molecules in allergic inflammation. g. g. side-effect profile). e. nose, lung, skin) Cytokines, chemokines, and adhesion molecules play a key role in regulating the immune and inflammatory responses during episodes of allergic inflammation Anti-IgE, leukotriene antagonists, and anti-IL-5 are examples of therapies that have targeted specific pathways associated with allergic inflammation Acknowledgement The authors acknowledge the contributions of Natalija Novak, Thomas Bieber and Patrick G Holt (Ch.