Innate immunity

We encounter microbes at every second but at most of the time, we never knew they were here. This is because most pathogens never get past our innate immunity. Innate immunity does not discriminate specific kinds of pathogens. It is thus said to be nonspecific. The first battle microbes have to fight against is the physical and chemical barriers. The second line of defense includes phagocytosis and inflammation. The table below illustrates how some nonspecific barriers and responses work.

Adaptive immunity

Very few pathogens make it past the defenses of our innate immunity and successfully colonize the body. If they do, then they are specifically targeted by the cells of our adaptive immunity and are usually cleared from the body.

Unlike the innate defense system, specific immune response is tailored to fight against each particular pathogen when they attack. Specific immune response is diverse and has the ability to evolve to attack unpresidented pathogens. Our body also gain memories from previous attacks so that when the same kind of pathogen invade again, it initiates a much faster secondary immune response. These characteristics enable specific immune response to be so effective against pathogens and to protect our body.

Immune system

The lymph vessels collect lymph from around the body eventually to lymph nodes. Phagocytes and lymphocytes are stationed at the lymph nodes, screening out pathogens from the lymph before the fluid return to the blood circulation.

Cells in the immune system originate in the bone marrow. They later differentiate into B lymphocytes and T lymphocytes. B lymphocytes mature in the bone marrow and the T lymphocytes mature in the thymus. Lymphocytes communicate with other cells and phagocytes using cytokines.

Antigen and antibodies

Antigens are large molecules like proteins and polysaccharides. Antigen on the cells of an organism is specific to itself. For example, Student A has antigen A on his blood cells while Student B has antigen B. Antigen A is self-antigen in Student A and antigen B is self-antigen to Student B. If blood cells of Student B enters Student A, antigen B is foreign to Student A. Foreign antigen is the cause of immune responses. One does not have antibodies against self-antigen but has antibodies against foreign antigen. Foreign antigens bind to antibodies that has the corresponding receptor, and trigger immune response by that attachment. The immune system responds by attacking foreign antigens. In the above case, Student A has antibodies against antigen B. Antigen B binds to Student A’s antibodies. The entry of blood cells of Student B thus triggers immune response of Student A.

Antigen presentation

Helper T cells (T_H cells) and cytotoxic T cells (T_C cells, or killer T cells) are mature and differentiated versions of T lymphocytes. T_H cells have surface protein CD4 whereas T_C cells have CD8. CD4 and CD8 are T-cell receptors that recognize and bind to antigen. When an antigen is bind to one of these T-cell receptors, T_H cells are activated to carry out an immune response.

In order for antigens to bind to the T-cell receptors and activate immune response, antigen-presenting cells (APC) are required to present the antigen to the T cells. APC include phagocytes and dendritic cells, which patrol the blood circulation, looking for, taking in and breaking down foreign particles. After breaking down the particles, fragments of foreign antigens are displayed on the surface of the APC, where they are then recognized by T_H cells.

Antigens are displayed on the surface of APC in particular ways, within a set of surface proteins called the major histocompatibility complex (MHC). This complex of proteins is essential in the recognition of self versus foreign. There are two types of MHC. MHCI is present on all nucleated cells and displays self antigens. MHCII is present on APC and displays foreign antigens.

Activation and action of T cells

In addition to the presentation of foreign antigen at the MHCI of APC to T_H cells, costimulatory signals are produced by APC in order to activate T_H cells, hinting T_H cells that the foreign antigens may pose danger to the body. Activated T_H cells secretes cytokines to stimulate T_C cells and B cells to do their jobs.

When T_C cells receive cytokines from T_H cells, they are stimulated to divide and mature. Unlike T_H cells, T_C cells recognize and bind to antigen that is displayed in MHCI, which is present on the surface of almost all cells in the body. Typically, if a body cell is infected by pathogen, the antigen of the pathogen is taken as ‘self’ to the infected cell, thus shows fragments of foreign antigen on MHCI. T_C cells recognize these foreign antigen on MHCI and identify these cells as infected cells. T_C cells are stimulated to release perforin, a protein that create pores in the infected cell and allow destructive enzymes to enter the cell, causing cytolysis.

Activation and action of B cells

B cells produce antibodies against the invading pathogen upon activation.

There are two types of antigen that can activate B cells, T-dependent antigens and T-independent antigens. T-dependent antigens activate B cells upon cytokines released by T cells while T-independent antigens activate B cells do not. Although two kinds of activation both result in the production antibodies by B cells, the activation by T-dependent antigen result in a stronger response and the production of immunologic memory.

T-dependent antigens are processed by B cells and presented to T_H cells on its MHCII. The T_H cell recognizes and bind to the MHCII-antigen complex on the B cell, receives costimulatory signals, and release cytokines that stimulate B cells to proliferate and differentiate. This process is known as clonal selection and expansion of B cell. It produce a mass of B cells that respond to the particular antigen of the invading pathogen. Some of the B cells differentiate into antibody-producing cells called plasma cells, which are relatively short-lived. Other differentiate into long-lived memory B cells. These memory cells can proliferate and differentiate rapidly when encountering the targeted antigen the next time. The action will be discussed in detail in the future section.

Antibodies act on antigens in a few ways. Antibodies have more than one binding sites for antigens. They can bind to more than on antigen at one time. This clumping of antigens is called agglutination. Agglutination helps prevent the spread of pathogens and makes it easier for phagocytes to clean them up. When antibodies bind to the surfaces of pathogens, it also results in neutralization of the pathogen. Antibodies surround the pathogen and prevent it to bind to the host body cells. Antibody may also bind to the pathogen and make it easier to be taken up by phagocytes. Phagocytosis is facilitated by this action called opsonization.

The table below illustrate the structures and functions of the five classes of antibodies.

Vaccination

Vaccine contain weakened version of pathogen. These pathogens are non-invasive and do not pose danger to human body. By injecting these weakened pathogen into the body, the antigens trigger primary immune response. Memory T and B cells are produced in the primary immune response. If the vaccinated person is infected by the same pathogen again, secondary immune response is triggered. Pathogens are rapidly killed so that infected person suffer less severe symptoms.

Types of immunity

Active immunity

An active immunity is a resistance to pathogen invasion through the production of antibodies by the immune system.

Passive immunity

One gains passive immunity by the introduction of antibodies from a foreign source.

Natural immunity and Artificial immunity

Natural immunity is naturally acquired while artificial immunity is introduced with artificial methods.

Examples