produzieren es selbst

TGF-beta2, expressed mainly by eosinophils, is the predominant isoform expressed in severe asthma, and is associated with increased profibrotic responses.

These results indicated that TGF beta 1 mRNA was overexpressed in severe asthmatics and that the main source of the mRNA was eosinophils, suggesting that eosinophils play an important role in the pathogenesis not only of inflammation but also of structural changes, such as subepithelial fibrosis, in asthmatic airways.

Nutritional deficiency of zinc is widespread throughout developing countries, and zinc-deficient persons have increased susceptibility to a variety of pathogens. Zinc deficiency in an experimental human model caused an imbalance between Th1 and Th2 functions. Production of interferon-gamma and interleukin (IL)-2 (products of Th1) were decreased, whereas production of IL-4, IL-6, and IL-10 (products of Th2) were not affected during zinc deficiency. Zinc deficiency decreased natural killer cell lytic activity and percentage of precursors of cytolytic T cells. In HuT-78, a Th0 cell line, zinc deficiency decreased gene expression of thymidine kinase, delayed cell cycle, and decreased cell growth. Gene expression of IL-2 and IL-2 receptors (both alpha and beta) and binding of NF-kappaB to DNA were decreased by zinc deficiency in HuT-78. Decreased production of IL-2 in zinc deficiency may be due to decreased activation of NF-kappaB and subsequent decreased gene expression of IL-2 and IL-2 receptors.

This study clearly showed that zinc deficiency increases allergic eosinophilic inflammation, whereas dietary zinc supplementation attenuates its intensity.

There are remarkable parallels in the immunological changes during aging and zinc deficiency, including a reduction in the activity of the thymus and thymic hormones, a shift of the T helper cell balance toward T helper type 2 cells

Mal sicher durch den Fettstoffwechsel (Omega 3 , 6 , 7, 9) , Astragalus Wurzel, Royal Jelley, Honig, Sibirischer Ginseng, Ginko, Rhodiola.

Auch noch Intressant

http://www.medical-tribune.de/medizin/falldiskussion/artikeldetail/asthma-therapie-wird-noch-effektiver.html

Der Metabolit 15d-PGJ2 (Ist PGD2 nach andocken an CRTH2) ist um einiges Potenter das Haarwachstum zu blockieren. Das ist auch kein Wunder da PGD2 nur eine Halbwertszeit von wenigen Stunden hat.
15d-PGJ2 ist viel stabiler und wird wahrscheinlich nur sehr langsam abgebaut. Es wird ausgegangen das 15d-PGJ2 etwas noch tiggert da es nicht die Hauptursache zu sein scheint.

Ja ist nicht schlecht aber mir fehlt zu viel. Wie zb Einfluss vom Fettstoffwechsel, TH1/TH2, Immunsystem und vorallem Glutahoine.

The nonenzymatic metabolite of PGD2, 15-dPGJ2, was also increased in balding scalp compared to haired scalp (Fig. 2E). However, the absolute level of 15-dPGJ2 (3.8 ng/g bald scalp, 1.3 ng/g haired scalp) was lower than PGD2 (53.5 ng/g bald scalp, 25.6 ng/g haired scalp) (Fig. 2F).

Starting at 5 μM, PGD2 and 15-dPGJ2 significantly inhibited hair growth. At 10 μM, PGD2-treated hair was 62 ± 5% shorter than vehicle, whereas 10 μM 15-dPGJ2 completely inhibited all hair growth.

Es tiggert Capascade 3 welches den Zelltot einleitet.

lest euch den beitrag von GansterBoy durch. sehr interessante hypothese. vielleicht stehen wir ja wirklich knapp vor des rätsels lösung!!!
http://www.hairlosshelp.com/forums/messageview.cfm?catid=7&threadid=103373&enterthread=y