By S. Holgate, et. al.
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B) In genome-wide approaches (whether by linkage analysis in families or by genome-wide association studies), genetic variation across the genome is genotyped to identify a genetic region that underlies disease susceptibility. The genes in the region can then be identified and how their encoded products contribute to disease pathogenesis established. disease in question, it does require considerable molecular genetic analysis to be undertaken in large family cohorts, involving considerable time, resources, and expense.
Atopic asthma has also been widely studied, and both twin and family studies have shown a strong heritable component to this phenotype, although estimates of the contribution of genetics to atopy and allergic disease susceptibility vary widely from 40 to >80% and it is apparent that the genetic contribution to risk of allergic disease such as asthma (λSib ~2–3) is weaker than that of other common conditions such as rheumatoid arthritis (λSib 8), type 1 diabetes (λSib 14) and Crohn disease (λSib 30) .
Anti-IgE inhibits both the EPR as well as the LPR response in the lung. Interestingly, anti-IL-5 does not significantly inhibit the LPR response to allergen challenge. 5 1 2 3 4 5 6 7 Time (h) 8 9 10 11 12 24 Fig. 31 Early and late phase responses in asthma. The asthmatic response to allergen inhalation challenge with house dust mite allergen (green line) and diluent control (red line), demonstrating both an early and a late phase allergic response. FEV1, forced expiratory volume in 1 second. EPR and LPR in the nose In the nose, topical allergen challenge of sensitized individuals causes immediate nasal reactions involving itching, sneezing, congestion, and watery discharges.