Serum IL-4 in atopic asthmatics was significantly elevated compared with nonatopic asthmatics. (2.35 ± 0.26 pg/ml vs 1.56 ± 0.12 pg/ml, p < 0.005). Interleukin 4 in sera from nonatopic asthmatics significantly increased beyond that in the controls (p < 0.05). Serum sIL-2R and sFceRII were essentially the same in the two asthmatic groups (Table 2).
Search for IgE Correlation With IL-4 or sFceRII in Asthmatics
Serum IL-4 did not correlate with total IgE in asthmatics (r = 0.30) (Fig 3). Also as to sFceRII, the same result was obtained (r = 0.03) (Fig 4).
Bronchial mucosal inflammation may possibly give rise to asthma symptoms. T cells may have some role in inflammatory response which is antigen driven since these cells recognize and respond directly to antigens. www.canadian-familypharmacy.com
Some molecules, such as IL-2R, class II MHC molecules, and VLA molecules, appear and increase in number on the surface of T cells following activation by a specific antigen. The expression of these molecules on T cells at sites of inflammation indicates that they are activated and are secreting lymphokines. The receptor for IL-2, a lymphokine produced by activated T cells and essential for their own continued proliferation, appears on the surface of T cells about 24 h after activation. In the absence of antigenic exposure, it continues to be present for several days and then disappears. Measurement of its soluble fragment is applied to assess various diseases.
SIL-2R and IL-4 are generated by T cells, sFceRII mainly are derived from В cells and may possibly be a В-cell activation marker. They were found in this study to increase in asthmatics. A weak but significant correlation of sIL-2R with sFceRII was observed. Constant allergen exposure to bronchial mucosa would thus appear to induce T-cell activation with subsequent lymphokine production, signal transduction to В cells, and continuous В-cell activation in asthmatics.
Interleukin 4, a T-cell-derived glycoprotein of 20 kDa, causes activation, proliferation, and differentiation of В cells and enhances the expression of class II MHC on the same cell type. Interleukin 4 plays a key role in isotype switching in murine and human В-cell antibody response. Thus, IL-4 is recognized to be an essential factor in the pathogenesis of allergic disease, such as atopic dermatitis, rhinitis, and asthma.
Table 2 — Three Parameters of the Two Asthmatic Groups and the Control Group
|sIL-2R, U/ml||405.2 ±24.1||497.2 ± 48.5||251.5 ± 10.0|
|IL-4, pg/ml||2.35 ± 0.26*||1.56 ± 0.12f||1.08 ±0.15|
|FceRII, U/ml||314.3 ± 19.4||312.4 ±29.2||228.8 ± 6.7|
Figure 3. Correlation between serum IL-4 and total IgE in asthmatics. There was no significant correlation.
Figure 4. Correlation between serum sFceRII and total IgE in asthmatics. There was no significant correlation.