Serum data
For both the whole schizophrenic and control group as well as both female groups, no common model could be found due to having different influencing factors for serum IL-2 in these groups.
Whole SCH vs. whole CON
The complete model enabled an explication of 100% serum IL-2 variance in the whole control group, but not in the schizophrenic one (whole CON: F = 15375.15, p < .001; whole SCH: F = 1.17, p = .35). TNF-α dominated over the others included in the model and made a clear contribution to serum IL-2 variance in controls (t = 9.88, p < .001). Besides, IFN-γ tended to be able to predict serum IL-2 variance significantly in controls (t = 1.50, p = .08).
A model keeping TNF-α, cortisol, and estradiol showed that (1) cortisol was the primary contributor for serum IL-2 in schizophrenics and (2) estradiol also played a secondary role in
this regard, although the new model was only able to envisage 13% variance of serum IL-2 (whole SCH: F = 2.99, p = .04; cortisol: t = -2.44, p = .02; estradiol: t = -1.78, p = .08).
Male SCH vs. male CON
Similar findings were obtained for healthy males; (1) the model explained 100% serum IL-2 variance and (2) TNF-α was the primary influencing factor among those included in the model (♂CON: F = 16692.27, p < .001; TNF-α: t = 10.00, p < .001). In addition, IL-10 tended to have a noticeable effect on serum IL-2 in male controls (t = -1.85, p = .08). Nevertheless, no single parameter assessed in this study was able to make a significant prediction of serum IL-2 in male schizophrenics.
Female SCH vs. female CON
For both female groups, no common model could be found since serum IL-2 of both groups obviously had diverse influencing factors. However, an individual model dropping age for schizophrenic females showed that (1) estradiol, testosterone, cortisol, and IL-4 could significantly predict serum IL-2, (2) that IL-6 tended to be able to forecast IL-2 sufficiently, and (3) the model was able to explain 84% of serum IL-2 variance (♀SCH: F = 8.06, p = .03; estradiol: t = -6.17, p = .004; testosterone: t = 4.08, p = .02; cortisol: t = -3.52, p = .02; IL-4: t = 3.40, p = .03; IL-6: t = -2.51, p = .07). A model keeping IFN-γ, TNF-α, IL-4, cortisol, and testosterone for control females was found. It exhibited a single dominant predictor TNF-α for serum IL-2. However, the new model could explicate only 20% IL-2 variance (♀CON: F = 2.62, p = .05; TNF-α: t = 2.13, p = .04).
Summary Summary Summary Summary:
(1) TNF-α was the dominant factor in the whole control group, whereas cortisol was the essential one in the whole schizophrenic group in envisaging serum IL-2. The explainable portion of serum IL-2 through the predictors included was only 13% in the schizophrenic group.
(2) TNF-α was the only important contributor of serum IL-2 in male controls, while none of those parameters assessed made a significant contribution to serum IL-2 in schizophrenic men. Serum IL-2 variance in male schizophrenics was impossible to be reliably explained by any of the parameters assessed in this study.
(3) TNF-α was crucial in predicting serum IL-2 in female controls, However, estradiol, testosterone, cortisol, and IL-4 were important in this regard in schizophrenic women. The explainable part of serum IL-2 variance was 84% in female schizophrenics.
Whole blood assay data
The complete model could predict whole blood assay IL-2 variance reliably in all groups but female schizophrenics (whole SCH: F = 9.45, p < .001; whole CON: F = 4.06, p < .001;
♂SCH: F = 11.20, p < .001; ♂CON: F = 3.10, p = .03; ♀CON: F = 3.22, p = .009; ♀SCH: F = 2.04, p = .30).
Whole SCH vs. whole CON
TNF-α played a dominant role in envisaging whole blood IL-2 in vitro production in both the whole schizophrenic and control group (whole CON: t = 7.50, p < .001; whole SCH: t = 4.01, p < .001). IL-6 and age also tended to have marked impacts on whole blood assay IL-2 release in schizophrenics and controls, respectively (whole CON – IL-6: t = -1.81, p = .08; whole SCH – age: t = 1.83, p = .08). Furthermore, the explainable portions of whole blood assay IL- 2 were 57% and 62% for schizophrenics and controls, correspondingly.
Male SCH vs. male CON
The results from male patients were similar to those of the whole schizophrenic group. TNF-α was the major contributor and age tended to make a significant contribution to whole blood assay IL-2 variance (TNF-α: t = 3.23, p < .001; age: t = 1.81, p = .09). In contrast to the findings in the whole control group, a series of variables were involved or tended to be involved in whole blood assay IL-2 release in male controls; they included TNF-α, IL-6, IFN-
γ, testosterone, age, and SHBG. Nevertheless, the model explicated similar portions of IL-2 variance in both male groups (♂CON: 75%; ♂SCH: 72%).
Female SCH vs. female CON
Similar outcomes were gained from female controls; TNF-α was the primary “donor” of whole blood IL-2 in vitro secretion and, additionally, prolactin likewise tended to exert a marked influence on IL-2 (TNF-α: t = 4.03, p = .001; prolactin: t = 1.80, p = .09).
A reduced model dropping IL-6, age, and cortisol improved the envisaging reliability of the predictors in schizophrenic women. However, the model also led to a change in control females (♀SCH: F = 5.35, p = .03; ♀CON: F = 4.54, p = .002). The new model explicated, instead of 62% by the complete model, only 46% whole blood assay IL-2 variance in female controls. It explained, nevertheless, 71% of IL-2 variance in schizophrenic females. TNF-α kept its dominant role in the new model in healthy females, while no single predictor alone could significantly predict whole blood IL-2 in vitro production in female subjects with schizophrenia (♀CON – TNF-α: t = 4.10, p < .001).
Summary Summary Summary Summary:
(1) TNF-α seemed to play an essential role in predicting whole blood IL-2 in vitro production in all groups but female schizophrenics.
(2) No single parameter was able to make a noticeable contribution to whole blood asssay IL-2 variance in schizophrenic women.