Remission of autoimmune diabetes by anti-TCR combination therapies with anti-IL-17A or/and anti-IL-6 in the IDDM rat model of type 1 diabetes

Table 2 Pro-and anti-inflammatory cytokine gene expression by in situ RT-PCR in the islet immune cell infiltrate

Gene	Healthy control	Anti-TCR and anti-IL-6	Anti-TCR and anti-IL-17A	Anti-TCR, anti-IL-6 and anti-IL-17A	Diabetic control
TNF	0.0 ± 0.0	1.1 ± 0.1**	5.3 ± 0.3**	0.0 ± 0.0**	19.4 ± 0.6
IL1B	0.1 ± 0.0	0.8 ± 0.1**	6.8 ± 0.4**	0.0 ± 0.0**	23.7 ± 1.0
IFNG	0.0 ± 0.0	0.2 ± 0.1**	0.4 ± 0.1**	0.0 ± 0.0**	1.7 ± 0.2
IL2	0.0 ± 0.0	0.4 ± 0.1	0.8 ± 0.1	0.0 ± 0.0	2.8 ± 0.2
IL4	0.0 ± 0.0	0.1 ± 0.1	1.1 ± 0.1	0.0 ± 0.0	5.9 ± 0.4
IL10	0.0 ± 0.0	0.4 ± 0.1	0.9 ± 0.1	1.5 ± 0.3	3.1 ± 0.3
IL6	0.0 ± 0.0	0.0 ± 0.0**	2.0 ± 0.2*	0.0 ± 0.0**	5.6 ± 0.2
IL17A	0.0 ± 0.0	1.4 ± 0.2**	0.0 ± 0.0**	0.0 ± 0.0**	4.0 ± 0.2

Gene expression changes for the pro- and anti-inflammatory cytokines TNF (Tnf), IL1B (Il1b), IFNG (Ifng), IL2 (Il2), IL6 (Il6), IL17A (Il17a), IL4 (Il4) and IL10 (Il10) in the immune cells infiltrate of pancreatic islet 60 days after the end of different anti-TCR combination therapies with anti-IL-6 or anti-IL-17A alone or in triple fashion in the LEW.1AR1-iddm rats. Quantitatively, a percentage of the immune cell infiltrate area showing a positive mRNA transcript for the different cytokines was calculated in the pancreases of the successfully treated rats in all groups (a total of 50 to 80 islets in each group). *p < 0.05, **p < 0.01 by ANOVA followed by Dunnett’s test for all successful therapies against the diabetic controls. Numbers of pancreases analysed as given in Fig. 1

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