The adaptive immune response, also known as
acquired or specific immunity, is the body’s defense system tailored to target a specific
pathogen. It has two branches: cellular or cell-mediated
immunity, and humoral, or antibody-mediated immunity. The major players of cellular immunity are
T-lymphocytes. They develop in the thymus, for which they
are named. During the process of maturation, billions
of variations of T-cells are formed, each carrying a unique surface protein, called
T-cell receptor, TCR. In addition, a population of T-cells, called
helper T-cells, also has a receptor named CD4; while a second population, of cytotoxic
T-cells, carries CD8 receptor. In the process of development, T-cells also
learn to not react to the body’s own antigens; those that react to self-molecules are eliminated. Mature T-cells then migrate to lymph nodes
and other lymphoid tissues, where they await exposure to pathogens. Basically, specific immunity relies on the
invading pathogen finding a match among these billions of T-cell variations. Only the ones that can bind to the pathogen,
are selectively activated. T-cells, however, cannot bind free-floating
pathogens. They can only bind to pieces of the pathogen
bound to a certain host molecule called major histocompatibility complex, or MHC, on the
surface of so-called “antigen-presenting cells”. There are two classes of MHC:
- MHC class I molecules are expressed by all nucleated cells of the body. These molecules are constantly produced in
the cytoplasm and, on their way to the cell membrane, pick up pieces of peptides and display
them on the cell surface. If a cell is infected by a virus or is cancerous,
a foreign or an abnormal antigen is displayed; and the cell can bind and activate a matching
T-cell. MHC-I only binds CD8 receptor, thus activating
only cytotoxic T-cells. - MHC class II molecules occur exclusively
on professional antigen-presenting cells, of which dendritic cells are most effective. Resident dendritic cells on the site of infection
swallow up pathogens, cut them into pieces, and display them on MHC-II molecules on their
surface. These dendritic cells then migrate to the
nearest lymph node, where they present the antigens to a matching T-helper cell, whose
CD4 receptor binds to MHC-II. Activation of T-cells, however, requires a
second binding between the two cells. This is the verification step, a safeguard
mechanism serves to prevent the immune system from overreacting. Once activated, T-cells undergo repeated cycles
of mitosis in a process called clonal expansion. This process produces clones of identical
cytotoxic and helper T-cells, both of which are specific to the pathogen. Some of these cells differentiate into effector
cells, while other become memory cells. Most effector T-cells leave the lymph node
for the bloodstream and are delivered to the site of infection, where they carry out immune
attack against the pathogen. Helper T-cells produce interleukins which
help with the activation of cytotoxic T-cells, B cells, and other immune cells. With such diverse functions, helper T-cells
are central to adaptive immunity. Cytotoxic T-cells, on the other hand, are
the main actors of cellular immunity. They release toxins and directly kill infected
or cancerous host cells. While effector cells die during or shortly
after the infection, memory cells live for much longer periods of time. Some of them remain in lymph nodes, while
other circulate the blood or migrate to peripheral tissues. Memory T-cells are also more numerous than
the original naïve T-cells. Upon reexposure to the same pathogen, they
can mount a much faster immune response, destroying the pathogen so quickly that no signs of illness
are noticeable. It is important to note the role of a third
T-cell population, known as regulatory, or suppressor T-cells, in dampening the immune
response when it’s no longer needed. Once the pathogen is cleared, regulatory T-cells
downregulate the proliferation of effector T-cells, keeping the immune reaction from
running out of control. They also help differentiate between self
and non-self antigens, and thus preventing autoimmune diseases.
