Humoral vs Cell mediated Immunity- Definition, 20 Differences
The immune system is a complex network of cells, tissues, and organs that protect the body from harmful pathogens and foreign substances. The immune system can be divided into two main branches: humoral immunity and cell-mediated immunity. Both types of immunity are essential for defending the body against different kinds of threats, but they have different mechanisms and functions.
Humoral immunity and cell-mediated immunity are two types of adaptive immune responses that protect the body from different kinds of pathogens and foreign substances. They differ in their characteristics such as:
- The type of antigens they recognize
- The type of immune cells they involve
- The type of effector molecules they produce
- The type of memory they generate
The following table summarizes the main characteristics of humoral immunity and cell-mediated immunity:
|Immune cell type
|Effector molecule type
|Memory B cells
|Memory T cells
Humoral and cell-mediated immunity are two types of adaptive immune responses that help the body fight against different kinds of pathogens. They have some similarities, such as involving lymphocytes and antigen recognition, but they also have some important differences. Here are 20 differences between humoral and cell-mediated immunity:
|An antibody-mediated response that occurs when foreign antigens are detected in the body fluids.
|A response that does not depend on antibodies but involves the activation and proliferation of T lymphocytes, macrophages and cytokines.
|Main cells involved
|B lymphocytes (plasma cells and memory B cells)
|T lymphocytes (helper T cells, cytotoxic T cells and memory T cells)
|B cells recognize free antigens in the blood or lymph.
|T cells recognize antigens presented by antigen-presenting cells (APCs) such as macrophages, dendritic cells or B cells.
|B cells act as APCs and present antigens to helper T cells using MHC class II molecules.
|APCs present antigens to helper T cells using MHC class II molecules and to cytotoxic T cells using MHC class I molecules.
|Activation of lymphocytes
|B cells are activated by helper T cells or by cross-linking of their surface immunoglobulins by antigens.
|T cells are activated by APCs and co-stimulatory signals such as cytokines or costimulatory molecules.
|Differentiation of lymphocytes
|Activated B cells differentiate into plasma cells that secrete antibodies or memory B cells that provide long-term immunity.
|Activated T cells differentiate into helper T cells that secrete cytokines or cytotoxic T cells that kill infected or abnormal cells or memory T cells that provide long-term immunity.
|Antibodies bind to antigens and neutralize them or mark them for destruction by phagocytes or complement system.
|Cytotoxic T cells release perforins and granzymes that induce apoptosis of target cells or secrete cytokines that activate macrophages or natural killer (NK) cells.
|Major histocompatibility complex (MHC) involved
|MHC class II molecules are involved in antigen presentation by B cells to helper T cells.
|MHC class I molecules are involved in antigen presentation by infected or abnormal cells to cytotoxic T cells. MHC class II molecules are involved in antigen presentation by APCs to helper T cells.
|Types of antigens involved
|Humoral immunity is effective against extracellular antigens such as bacteria, toxins, viruses in the blood or lymph.
|Cell-mediated immunity is effective against intracellular antigens such as viruses, bacteria or parasites inside the cells or tumor antigens or transplant antigens on the cell surface.
|Types of antibodies involved
|Humoral immunity involves different classes of antibodies such as IgM, IgG, IgA, IgE and IgD. Each class has a different function and distribution in the body.
|Cell-mediated immunity does not involve antibodies but relies on cell-to-cell interactions and cytokine signaling.
|Primary response time
|Humoral immunity develops quickly after the first exposure to an antigen. The peak antibody production occurs within 7 to 10 days. The antibody level then declines gradually.
|Cell-mediated immunity takes longer to develop after the first exposure to an antigen. The peak T cell proliferation occurs within 10 to 14 days. The T cell level then declines gradually.
|Secondary response time
|Humoral immunity produces a faster and stronger secondary response upon re-exposure to the same antigen due to the presence of memory B cells that can quickly differentiate into plasma cells and secrete high-affinity antibodies. The peak antibody production occurs within 3 to 5 days. The antibody level remains high for a longer period of time.
|Cell-mediated immunity produces a faster and stronger secondary response upon re-exposure to the same antigen due to the presence of memory T cells that can quickly differentiate into effector T cells and mount a rapid and specific attack on the target cells. The peak T cell proliferation occurs within 5 to 7 days. The T cell level remains high for a longer period of time.
|Humoral immunity provides immunological memory by generating long-lived memory B cells that can recognize and respond to the same antigen upon re-exposure.
|Cell-mediated immunity provides immunological memory by generating long-lived memory T cells that can recognize and respond to the same antigen upon re-exposure.
|Immunoglobulin class switching
|Humoral immunity involves immunoglobulin class switching, which is the process of changing the antibody class produced by a B cell without altering its antigen specificity. This allows the B cell to produce different classes of antibodies depending on the type and location of the antigen and the stage of the immune response.
|Cell-mediated immunity does not involve immunoglobulin class switching, as it does not depend on antibodies.
|Humoral immunity involves affinity maturation, which is the process of increasing the binding affinity of antibodies to their specific antigens over time. This occurs through somatic hypermutation and selection of B cells with higher-affinity antibodies in the germinal centers of lymphoid tissues.
|Cell-mediated immunity does not involve affinity maturation, as it does not depend on antibodies.
|Humoral immunity is responsible for type I, type II and type III hypersensitivity reactions, which are allergic or autoimmune responses that occur when antibodies bind to antigens and cause inflammation, tissue damage or anaphylaxis.
|Cell-mediated immunity is responsible for type IV hypersensitivity reaction, which is a delayed-type hypersensitivity response that occurs when T cells or macrophages react to antigens and cause inflammation, tissue damage or granuloma formation.
|Humoral immunity can be impaired by immunodeficiency diseases that affect the production or function of B cells or antibodies.
|Cell-mediated immunity can be impaired by immunodeficiency diseases that affect the production or function of T cells or macrophages.
|Humoral immunity can be induced by active immunization or passive immunization methods.
|Cell-mediated immunity can be induced by active immunization methods only.
|Role in cancer immunity
|Humoral immunity plays a limited role in cancer immunity, as most tumor antigens are intracellular and not accessible to antibodies.
|Cell-mediated immunity plays a major role in cancer immunity, as cytotoxic T cells can recognize tumor-associated antigens on the surface of cancer cells and induce apoptosis of them.
|Role in transplantation immunity
|Humoral immunity plays a role in transplantation immunity, as antibodies can recognize foreign antigens on the surface of transplanted organs or tissues and cause hyperacute rejection or chronic rejection.
|Cell-mediated immunity plays a role in transplantation immunity, as T cells can recognize foreign antigens on the surface of transplanted organs or tissues and cause acute rejection or chronic rejection.
Humoral and cell-mediated immunity are two types of adaptive immune responses that protect the body from foreign antigens. Humoral immunity involves the production of antibodies by B cells, while cell-mediated immunity involves the activation of T cells. Both types of immunity are initiated by the recognition of antigens by specific receptors on B cells and T cells but differ in how they recognize antigens and how they are activated.
Humoral and cell-mediated immunity are both essential for the protection of the body against various pathogens and diseases. However, they have different roles and applications in different situations.
Humoral immunity is mainly effective against extracellular pathogens, such as bacteria, viruses, fungi, and parasites that are present in the body fluids. Humoral immunity can also prevent the re-infection by the same pathogen by producing memory B cells that can quickly produce specific antibodies upon exposure. Humoral immunity is also involved in allergic reactions, autoimmune diseases, and transplant rejection.
Cell-mediated immunity is mainly effective against intracellular pathogens, such as viruses, bacteria, and parasites that infect the cells of the body. Cell-mediated immunity can also eliminate abnormal or infected cells, such as cancer cells or cells infected with latent viruses. Cell-mediated immunity is also involved in delayed-type hypersensitivity reactions, contact dermatitis, and graft-versus-host disease.
The applications of humoral and cell-mediated immunity can be exploited for various purposes in medicine and biotechnology. For example:
- Monoclonal antibodies
These are some of the applications of humoral and cell-mediated immunity in various fields of science and medicine. Humoral and cell-mediated immunity are both important components of the adaptive immune system that work together to defend the body against a wide range of threats. Understanding their differences and similarities can help us appreciate their functions and potential uses.
We are Compiling this Section. Thanks for your understanding.