Poster Presentation The 13th International Congress of the Immunology of Diabetes Society 2013

Proliferating germinal centres are decreased in recent onset type 1 diabetes pancreatic lymph nodes (#127)

Abby Willcox 1 , Sarah J Richardson 2 , Lucy S K Walker 3 , Noel G Morgan 2 , Kathleen M Gillespie 1
  1. University of Bristol, Bristol, United Kingdom
  2. University of Exeter Medical School, Exeter, United Kingdom
  3. Institute of Immunity and Transplantation, UCL Medical School, London, United Kingdom


Pancreatic lymph nodes (PLN) at the periphery of the pancreas, propagate the autoimmune response and have been understudied in type 1 diabetes (T1D). The aim of this study was to analyse the structure and cellular content of secondary B cell follicles (germinal centres (GC)) in recent-onset T1D compared with matched controls. 

Materials and Methods

8 PLNs from 6 donors with recent onset T1D (<1 year duration) and 10 PLNs from 8 non-diabetic donors were stained for the proliferation marker Ki67. GCs were identified based on ≥3 Ki67+ cells within a B cell follicle (CD20+ cells). The area of each PLN examined was measured with ImageJ software.


In the control group, 8 proliferating GCs were observed in 6 PLNs; each containing between 4-227 Ki67+ cells (mean 72.3±23.6). The Ki67+ GC cells accounted for 11.7-75.9% of all cells within the B cell follicle (mean 43.6±7.1%). Unexpectedly, only one proliferating GC was identified in the PLNs of the recent onset T1D group and as this was on the edge of a section and it was not possible to quantify the cells accurately. The area of the PLNs examined was not statistically different between the groups (mean 3.1±0.8 mm2 (range 0.05-6.7 mm2) and (mean 5.4±2.1 mm2 (range 0.45-15.9 mm2); p=0.2 for the T1D and control group respectively).


Germinal centre replication is required for affinity maturation of the humoral immune response. Counter-intuitively, replication is decreased in GCs in recent onset T1D compared with non-diabetic controls.  These data may reflect burnout of the humoral response but this is not supported by the presence of insulitis in recent onset islets1 and post-diagnosis islet autoantibody production.  Another interpretation may be attempted regulation of the autoimmune response in T1D PLNs. Further studies are required to understand the mechanisms underlying decreased Ki67+ GCs in T1D.

  1. A Willcox, SJ Richardson, AJ Bone, AK Foulis and NG Morgan. Analysis of islet inflammation in human type 1 diabetes. Clin Exp Immunol (2009) 155: 173-181.