Activated T cells work by recognizing and responding to specific antigens, orchestrating an immune response to eliminate threats. This process involves a series of complex interactions and specialized functions.
Here's a breakdown of how activated T cells function:
1. Antigen Recognition and Activation
- T Cell Receptor (TCR) Binding: The process starts when a T cell receptor (TCR) on the surface of the T cell binds to an antigen presented by an antigen-presenting cell (APC), such as a dendritic cell, B cell, or macrophage. This antigen is displayed on a Major Histocompatibility Complex (MHC) molecule. There are two main types of MHC molecules:
- MHC Class I: Presents antigens to cytotoxic T cells (also known as CD8+ T cells).
- MHC Class II: Presents antigens to helper T cells (also known as CD4+ T cells).
- Co-stimulatory Signals: Antigen recognition alone is not sufficient for full T cell activation. The T cell also requires co-stimulatory signals, which are delivered by interactions between molecules on the T cell and the APC. A key example is the interaction between CD28 on the T cell and B7 (CD80 or CD86) on the APC.
2. T Cell Differentiation and Proliferation
- Clonal Expansion: Once activated, the T cell undergoes clonal expansion, meaning it rapidly divides to create a large population of T cells that are specific for the same antigen.
- Differentiation into Effector Cells: Activated T cells differentiate into various effector T cell subtypes, each with a specialized function. The main types include:
- Cytotoxic T Lymphocytes (CTLs or CD8+ T cells): CTLs kill infected or cancerous cells that display the specific antigen recognized by their TCR on MHC class I molecules.
- Helper T cells (CD4+ T cells): Helper T cells secrete cytokines that activate other immune cells, such as B cells, macrophages, and other T cells. They are crucial for orchestrating adaptive immune responses. Different subsets of helper T cells exist, including:
- Th1 cells: Promote cell-mediated immunity and are important for fighting intracellular pathogens.
- Th2 cells: Promote humoral immunity (antibody production) and are important for fighting extracellular parasites.
- Th17 cells: Important for fighting extracellular bacteria and fungi.
- Treg cells: Suppress the immune response and maintain immune homeostasis, preventing autoimmunity.
3. Mechanisms of Action
- Cytotoxic T Lymphocytes (CTLs):
- Perforin and Granzymes: CTLs release perforin, which creates pores in the target cell membrane, and granzymes, which enter the target cell through these pores and induce apoptosis (programmed cell death).
- Fas-FasL Interaction: CTLs express Fas ligand (FasL) on their surface, which binds to Fas (also known as CD95) on the target cell surface, triggering apoptosis.
- Helper T Cells:
- Cytokine Secretion: Helper T cells secrete a variety of cytokines that activate other immune cells. For example, IFN-γ (secreted by Th1 cells) activates macrophages, while IL-4 (secreted by Th2 cells) promotes B cell antibody production.
- B Cell Help: Helper T cells provide crucial signals for B cell activation, proliferation, and differentiation into antibody-secreting plasma cells. This interaction typically occurs via CD40L on the T cell binding to CD40 on the B cell, along with cytokine secretion.
4. Memory T Cell Formation
- Long-lived Immunity: After the infection is cleared, most effector T cells die off, but a subset differentiates into memory T cells.
- Rapid Response: Memory T cells are long-lived and provide rapid and enhanced immune responses upon subsequent encounters with the same antigen. There are two main types of memory T cells:
- Central memory T cells (Tcm): Reside in lymphoid organs and are important for long-term immunity.
- Effector memory T cells (Tem): Circulate in peripheral tissues and provide rapid effector functions upon re-encounter with the antigen.
Example
Imagine a virus infecting a cell. The infected cell presents viral antigens on MHC class I molecules. A CTL with a TCR specific for this viral antigen will bind to the MHC-antigen complex and receive co-stimulatory signals. This activates the CTL, causing it to proliferate and differentiate into an effector CTL. The effector CTL then finds and kills other infected cells presenting the same viral antigen by releasing perforin and granzymes or by interacting with Fas on the infected cell.
