Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. Activated B lymphocytes up-regulate ALCAM upon both BCR- and TLR-dependent activation.
  • Fig. S2. ALCAM expression on peripheral and CNS-infiltrating B lymphocytes is increased during the course of MOG35–55–EAE.
  • Fig. S3. ALCAM+ B lymphocytes are preferentially localized in meningeal infiltrates in EAE.
  • Fig. S4. Few immune cells and B lymphocytes are isolated from the CNS of naïve WT mice.
  • Fig. S5. CNS-infiltrating B lymphocytes do not coexpress cell adhesion molecules in EAE.
  • Fig. S6. Immune cells infiltrate CNS of ALCAM KO and WT mice during the chronic phase of the disease.
  • Fig. S7. Absolute numbers of B lymphocytes are similar in lymphoid organs of ALCAM KO and WT mice in the presymptomatic phase.
  • Fig. S8. Non–B lymphocyte immune cell migration into the CNS is not affected by ALCAM blockade in B lymphocyte–dependent rhMOG EAE model.
  • Fig. S9. ALCAM promotes the migration of human B lymphocytes across CNS barriers and is up-regulated in relapsing patients with MS.
  • Fig. S10. ALCAM mediates the adhesion of human B lymphocytes on BBB endothelium.
  • Fig. S11. Cell adhesion molecules are coexpressed on ex vivo B lymphocytes from PBMCs of patients with MS.
  • Fig. S12. Most CD20+ cells in MS brain immune infiltrates are not CD3+ cells.
  • Fig. S13. Cell adhesion molecules are coexpressed on B lymphocytes in MS lesions.
  • References (7582)

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