American Society of Hematology

Figure 1

$Figure 1. Measurement of T-cell repertoire oligoclonality in human clinical GVHD samples. (A) Diagram of sample collection for patients. (B) GI tissue samples from primary-responsive (PR; n = 8) and steroid-refractory (SR; n = 7) patients show the same - cell repertoire oligoclonality as measured by the Gini coefficient (Mann-Whitney, P = .5893). Comparison is of patient averages of individual tissue samples. (C) Blood samples from PR and SR patients at time of diagnosis (●) and day +30 after diagnosis (○) show the same T-cell repertoire oligoclonality (Mann-Whitney, P = .1919). (D) GI tissue samples do not show increased T-cell repertoire oligoclonality with increased GVHD histology grade. Comparison is of average Gini coefficients per patient at each histology grade (Kruskal-Wallis, P = .2600). (E) No significant change in oligoclonality in the blood between the day of diagnosis and day +30 after diagnosis for either PR or SR patients (Wilcoxon, P = .2188).$

Measurement of T-cell repertoire oligoclonality in human clinical GVHD samples. (A) Diagram of sample collection for patients. (B) GI tissue samples from primary-responsive (PR; n = 8) and steroid-refractory (SR; n = 7) patients show the same - cell repertoire oligoclonality as measured by the Gini coefficient (Mann-Whitney, P = .5893). Comparison is of patient averages of individual tissue samples. (C) Blood samples from PR and SR patients at time of diagnosis (●) and day +30 after diagnosis (○) show the same T-cell repertoire oligoclonality (Mann-Whitney, P = .1919). (D) GI tissue samples do not show increased T-cell repertoire oligoclonality with increased GVHD histology grade. Comparison is of average Gini coefficients per patient at each histology grade (Kruskal-Wallis, P = .2600). (E) No significant change in oligoclonality in the blood between the day of diagnosis and day +30 after diagnosis for either PR or SR patients (Wilcoxon, P = .2188).

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