The innate response is typically enough to resolve the vast majority of infections.
For the minority of cases for which it doesn’t quite suffice, the adaptive response enters the picture. This is where we have B cells generating antibodies, and T cells making cytokines and killing infected cells.
Also at the site of infection are immature dendritic cells. These immune cells bridge the innate response with the adaptive response. They take a snapshot of the pathogen and go off to find help.
An immature dendritic cell “eats” the pathogen, processing the resulting antigens (broken down protein components of the pathogen) for presentation, and traveling to the lymph node.
At the lymph node, the dendritic cell encounters T cells. T cells are activated with the help of three signals.
Signal 1: Pathogen-derived antigen is loaded onto a protein-based molecule called a major histocompatibility complex (MHC), which is expressed at the surface of the dendritic cell and presents antigen to the T cell’s T cell receptor. If there is a match, wherein the T cell receptor recognizes the MHC-presented antigen, the T cell initiates its first activation signal internally.
Signal 2: Co-stimulation occurs, wherein molecules on the dendritic cell (like B7) interact with molecules on the T cell (like CD28), strengthening the antigen-specific interaction in the previous step. This leads to the T cell inducing increased expression of the cytokine IL-2, which drives proliferation of the T cell population and leads to expression of a molecule called CD40L on the T cell surface.
Signal 3: The dendritic cell produces cytokines that shape the T cell’s ultimate function. Often, IL-12 and IL-18 will be produced, both of which can act upon the T cell that the dendritic cell is interacting with.
There are two types of T cells, which are defined by the type of glycoprotein co-receptor expressed at their surface – CD4 and CD8 T cells.
The two types of T cells differ in terms of mechanism of activation.
For signal 1, depending on whether a CD4 or CD8 T cell is being activated, the dendritic cell will have to present pathogen-derived antigen on a distinct MHC. This is because the receptors on CD4 and CD8 T cells recognize antigen that is presented on distinctly shaped MHCs. CD4s recognize presentations from MHC class 2
The two are also vastly different in terms of function.
CD4 T cells – also termed T “helper” cells – will release distinct cytokines upon recognition of a target cell displaying the antigen it previously recognized on the dendritic cell.
CD8 T cells – also termed T “killer” cells – will release perforin and granzyme onto target cells (typically infected) that display the antigen it previously recognized on the dendritic cell. Perforin pokes holes in the membrane of the infected cell, providing a point of entry for granzyme, which drives apoptosis in the cell.
This article’s content was created based upon the background accrued over the course of the author’s Honours BSc Degree in Microbiology & Immunology, which included Immunology, Virology, and Bacterial Pathogenesis course-work and exposure to topics from Janeway’s Immunobiology.
