HUMORAL IMMUNITY
ACQUIRED IMMUNITY
In addition to its generalized innate immunity, the human body has the ability to develop extremely powerful
specific immunity against individual invading agents such as lethal bacteria, viruses, toxins, and even foreign
tissues from other animals. This ability is called acquired or adaptive immunity.
Acquired immunity is caused by a special immune system that forms antibodies and/or activated lymphocytes
that attack and destroy the specific invading organism or toxin. It is with this acquired immunity mechanism
and some of its associated reactions, especially the allergies.
Acquired immunity can often bestow an extreme degree of protection. For instance, certain toxins, such as
the paralytic botulinum toxin or the tetanizing toxin of tetanus, can be protected against in doses as high as
100,000 times the amount that would be lethal without immunity. It is for this reason that the treatment
process known as immunization is so important in protecting human beings against disease and against
toxins.
HUMORAL IMMUNITY
Humoral immunity is mediated by circulating immunoglobulin antibodies in the γ-globulin fraction of the
plasma proteins. Immunoglobulins are produced by differentiated forms of B lymphocytes known as
plasma cells, and they activate the complement system and attack and neutralize antigens (Figure 3–
1). Humoral immunity is a major defense against bacterial infections.
Humoral immunity is the aspect of immunity that is mediated by macromolecules – including secreted
antibodies, complement proteins, and certain antimicrobial peptides – located in extracellular fluids.
Humoral immunity is named so because it involves substances found in the humors, or body fluids. It
contrasts with cell-mediated immunity. Humoral immunity is also referred to as antibody-mediated
immunity.
PREPROCESSING OF B- LYMPHOCTES-a
much lesser known fact
Liver and bone marrow preprocess the B lymphocytes. In humans, B lymphocytes are known to be
preprocessed in the liver during midfetal life and in the bone marrow during late fetal life and after birth.
B lymphocytes are different from T lymphocytes in two ways -:
1)Instead of the whole cell developing reactivity against the antigen, as occurs for the T lymphocytes, the B
lymphocytes actively secrete antibodies that are the reactive agents. These agents are large proteins that are
capable of combining with and destroying the antigenic substance.
2) The B lymphocytes have even greater diversity than the T lymphocytes, thus forming many millions of
types of B lymphocyte antibodies with different specific reactivities. After preprocessing, the B lymphocytes,
like the T lymphocytes, migrate to lymphoid tissue throughout the body, where they lodge near but are
slightly removed from the T lymphocyte areas.
MECHANISM OF HUMORAL
IMMUNITY
1) PRESENTATION OF ANTIGEN
2) ACTIVATION OF B CELL
3) DIFFERENTIATION OF B CELL INTO PLASMA CELL
4) PROLIFERATION OF PLASMA CELLS AND
ANTIBODY PRODUCTION
5) KILLING OF THE INVADER BY ANTIBODIES THT
INCLUDE ACTIVATION OF COMPLEMENT SYSTEM
6) FORMATION OF MEMORY B CELLS AND
SUBSEQUENT IMMUNOLOGICA; RESPONSE
PRESENTATION OF ANTIGEN
APCs include specialized cells called dendritic cells in the lymph nodes and spleen
and the Langerhans dendritic cells in the skin. Macrophages and B cells themselves,
and likely many other cell types, can also function as APCs.
For example, in the intestine, the epithelial cells that line the tract are likely important
in presenting antigens derived from commensal bacteria.
In APCs, polypeptide products of antigen digestion are coupled to the HLA protein
products of the major histocompatibility complex (MHC) genes and presented on the
surface of the cell.
ACTIVATION OF B CELLS
B cells can bind antigens directly, but they must contact helper T cells to produce full activation and antibody
formation. It is the Th2 subtype that is mainly involved.
Helper T cells develop along the Th2 lineage in response to IL-4 (see below). On the other hand, IL-12 promotes
the Th1 phenotype. IL-2 acts in an autocrine fashion to cause activated T cells to proliferate.
The activated B cells proliferate and transform into memory B-cell & plasma cells.
The plasma cells secrete large quantities of antibodies into the general circulation. The antibodies circulate in
the globulin fraction of the plasma and, like antibodies elsewhere, are called immunoglobulins. The
immunoglobulins are actually the secreted form of antigen-binding receptors on the B cell membrane.
B Cells are also activated by MHC-AG
MHC-1 AND MHC-2
Major histocompatibility cells, are self antigens that help
identifying and rejecting foreign antigens .
DIFFERENTIATION OF B CELLS INTO
PLASMA CELLS
The activated B cell enlarges in size that undergoes complete transformation to become
plasma cell.
1. The cell is transformed completely in structure and function
2. Plasma cell has larger cytoplasm containing numerous RER
3. The enlarged B cell appears almost like a lymphoblast,sometimes this differentiaition is
called as blast transformation.(leukamia) Co stimulation by T helper cells (th2) facilitates
the process of transformation.
Formation of “memory” cells—enhances the
antibody response to subsequent antigen exposure.
A few of the lymphoblasts formed by activation of a clone of B lymphocytes do not go on
to form plasma cells but instead form moderate numbers of new B lymphocytes similar to
those of the original clone.
They also circulate throughout the body to populate all the lymphoid tissue;
immunologically, however, they remain dormant until activated once again by a new
quantity of the same antigen. These lymphocytes are called memory cells.
Subsequent exposure to the same antigen will cause a much more rapid and much more
potent antibody response this second time around because there are many more
memory cells than there were original B lymphocytes of the specific clone.
Proliferation of plasma cells and antibody
production
Before exposure to a specific antigen, the clones of B lymphocytes remain dormant in the lymphoid tissue. Upon
entry of a foreign antigen, macrophages in lymphoid tissue phagocytize the antigen and then present it to adjacent B
lymphocytes.
In addition, the antigen is presented to T cells at the same time, and activated T-helper cells are formed. These
helper cells also contribute to extreme activation of the B lymphocytes, The B lymphocytes specific for the antigen
immediately enlarge and take on the appearance of lymphoblasts.
Some of the lymphoblasts further differentiate to form plasmablasts, which are precursors ofplasma cells. In the
plasmablasts, the cytoplasm expands and the rough endoplasmic reticulum vastly proliferates.
The plasmablasts then begin to divide at a rate of about once every 10 hours for about 9 divisions, giving in 4 days a
total population of about 500 cells for each original plasmablast. The mature plasma cell then produces gamma
globulin antibodies at an extremely rapid rate—about 2000 molecules/second for each plasma cell. In turn, the
antibodies are secreted into the lymph and carried to the circulating blood. This process continues for several days
or weeks until finally exhaustion and death of the plasma cells occur.
ANTIBODIES
Antibodies are gamma globulins called immunoglobulins (Ig), that have molecular weights between
160,000 and 970,000 and constitute about 20% of all the plasma proteins.
All the Igs are composed of combinations of light and heavy polypeptide chains. Most are a combination
of two light and two heavy chains, a However, some of the Igs have combinations of as many as 10
heavy and 10 light chains, which give rise to high-molecular-weight Igs.
Yet, in all Igs, each heavy chain is paralleled by a light chain at one of its ends, thus forming a heavy–
light pair, and there are always at least 2 and as many as 10 such pairs in each Ig molecule. n. The
variable portion is different for each specific antibody, and it is this portion that attaches specifically to a
particular type of antigen.
The constant portion of the antibody determines other properties of the antibody, establishing such factors
as antibody diffusivity in the tissues, adherence of the antibody to specific structures within the tissues,
attachment to the complement complex, ease with which the antibodies pass through membranes, and
other biological properties of the antibody. A combination of noncovalent and covalent bonds (disulfide)
holds the light and heavy chains together.
KILLING OF INVADERS
Direct action of antibodies on invading agents. Because of the bivalent nature of the antibodies and the multiple antigen sites
on most invading agents, the antibodies can inactivate the invading agent in one of several ways, as follows:
1. Agglutination, in which multiple large particles with antigens on their surfaces, such as bacteria or red cells, are bound
together into a clump; precipitation, in which the molecular complex of soluble antigen (eg, tetanus toxin) and antibody
becomes so large that it is rendered insoluble and precipitates.
2. Neutralization, in which the antibodies cover the toxic sites of the antigenic agent;
3. lysis, in which some potent antibodies are occasionally capable of directly attacking membranes of cellular agents and
thereby cause rupture of the agent.
4. Opsonization and phagocytosis: One of the products of the complement cascade, C3b, strongly activates phagocytosis by
both neutrophils and macrophages, causing these cells to engulf the bacteria to which the antigen–antibody complexes are
attached. This process is called opsonization. It often enhances the number of bacteria that can be destroyed by many
hundredfold.
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TYPES OF HUMORAL RESPONSE
Thank You
BY-GROUP 07
POSTER TEAM: MODEL TEAM:
1. DEVIKA 1. ANIRUDH
2. HAMSINI 2. arya
3. SOUMYA 3. VED
4. SHEETAL 4. ALIZA
5. AASHITA 5. niharika
6. RANJITHA 6. manoj
7. KRUPA 7. NIHAR PRESENTATION
8. SAMIKSHA 8. NESAR BY:
9. SNIGDHA 9. VAISHNAV SHRADDHA
10. selmer 10. HEMANTH
GAURAV
CO-ACTOR-SWAYM