| Popis: |
Primary adaptive immune responses are initiated in secondary lymphoid organs, such as spleen, lymph nodes, and Peyer’s patches. These lymphoid organs recruit naive lymphocytes1 as well as activated antigen-presenting cells (APCs)2, and facilitate lymphocyte activation, expansion, and differentiation. For example, infection of the lung with influenza virus leads to activation of pulmonary dendritic cells, which engulf local antigens and traffic to the draining mediastinal lymph node (MLN)3, where they home to the T cell area surrounding the high endothelial venules (HEVs) (Figure 1). Naive B and T cells are constantly recruited into the lymph node via these HEVs and rapidly become activated as they encounter cognate antigen on APCs. Activated lymphocytes subsequently expand and differentiate into effector cells. For T cells, this differentiation primarily occurs in the T cell zone. In contrast, B cells rapidly expand and are selected for high-affinity variants in the germinal centers (GCs) that develop on the border between the T cell area and the B cell follicle. As the immune response progresses, effector B and T cells leave the lymph node via the efferent lymphatics, which drain into the blood via the thoracic duct. Once in the blood, activated effector cells recirculate to sites of inflammation, including the original site of infection in the lung, and use their effector functions to combat infection. An important point of this model is that, while infection occurs locally in non-lymphoid organs, primary immune responses are initiated centrally in secondary lymphoid organs. This scheme is outlined in Figure 1. |
