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Figure 5


Fig. 5. The role of LFA-1–{alpha}-actinin-1 in LN entry and schematic overview of a LN. (A) Effect of β2-actinin-blocking peptide on the migration of mouse T cells into peripheral and mesenteric LNs. The figure shows the effect on lymphocyte migration into LNs of T cells treated with a blocking peptide that consists of the {alpha}-actinin-1 binding site on the β2 cytoplasmic tail (top panel) linked to membrane-penetrating peptide penetratin-1 (β2-actinin peptide) (Stanley et al., 2008). Mouse LN T cells that had been labelled with the fluorescent dyes CFSE or SNARF-1 were incubated for 30 minutes with either the β2-actinin-blocking peptide or, alternatively, control peptide or Hanks buffered salt solution (HBSS), and injected intravenously into the host for 30 minutes. The numbers of fluorescently labelled T cells that successfully transmigrated into either peripheral or mesenteric LNs were quantified. The β2-actinin-blocking peptide, but not control treatments, severely retarded LN entry, implying a major role for the intermediate-affinity integrin bound to {alpha}-actinin-1 in this crucial step. (B). Schematic overview of a LN. Leukocytes enter the LN either through the afferent lymph into the subcapsular sinus, or the blood flow through HEVs. T cells migrate in the T-cell zone, thereby contacting resident DCs, which may activate the T cells if they are expressing appropriate antigen. B cells migrate to their follicles seeking an antigen stimulus. As a subsequent stage in their stimulation they encounter T cells at the T-cell–B-cell boundary zone. After migrating through the LN, lymphocytes exit through the medullary sinus into the efferent lymph. The lower panel shows a scheme to highlight integrin dependency (or the lack thereof) during the journey of the lymphocyte through the LN. Green, HEV (entry); purple, T-cell area (intranodal migration and lymphocyte contacts); blue, B-cell area (intranodal migration and lymphocyte contacts); grey, medulla (exit).





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