Lymphoid tissue engineering: invoking lymphoid tissue neogenesis in immunotherapy and models of immunity.

The plasticity of the immune system is evident in the reorganization of secondary lymphoid organs during immune responses, lymphoid tissue neogenesis occurring during chronic inflammation or graft rejection, and the engineered lymphoid tissue formation induced by ectopic expression of single lymphoid tissue-associated genes. Approaches seeking to harness this plasticity for immunotherapy are under investigation, particularly by controlling immune cell recruitment and lymphoid tissue formation at tumor sites. By combining strategies from ectopic tissue induction models with methods from tissue engineering, new approaches for studying lymphoid tissue development and immunotherapy may be possible.

Inverse opal hydrogel-collagen composite scaffolds as a supportive microenvironment for immune cell migration.

Immunotherapies harness the inherent potential of the body to destroy foreign or infected cells, and are currently being investigated as treatments for cancer. One way to boost native immune responses might be to engineer ectopic lymphoid tissue, providing a supportive microenvironment for immune cell priming, and/or bringing together immune cells at a desired location (e.g.

Homeostatic lymphoid chemokines synergize with adhesion ligands to trigger T and B lymphocyte chemokinesis.

Homeostatic chemokines such as CCL19, CCL21, and CXCL13 are known to elicit chemotaxis from naive T and B cells and play a critical role in lymphocyte homing to appropriate zones within secondary lymphoid organs (SLO). Here we tested whether CCL21 and CXCL13 modulate murine lymphocyte motility in the absence of concentration gradients, using videomicroscopy to directly observe the migration of single cells. CCL21 treatment of T cells induced rapid polarization and sustained random migration with average speeds of 5.