Question 1 (700 words)
Describe activation of innate immunity as soon as the infectious agents start to colonize.
(10 marks)
The immune system has three layers of defense. These include physical and chemical
barriers, non-specific resistance and particular resistance to foreign pathogens. However,
non-specific resistance along with physical and chemical barriers are considered innate
immunity, whereas particular resistance implies acquired immunity.
Innate immunity refers to unspecific defensive mechanisms that take place immediately or
during hours after the emergence of an antigen in the body. This sort of immunity from
birth is also known to develop. Pathogens are generically recognized and responded by the
cells of the innate system, but, unlike the adaptive immune system, the hosts have no longlasting or protective immunity. Innate immunity includes barriers that prevent the entry in
your body of hazardous substances. This includes physical obstacles, such as skin, blood
molecules, and cells that fight foreign cells in your body. These barriers form the first line
and second line defense in the immune response. Innate immune system also recruiting
immune cells to sites of infection, through production of chemical factors, including
specialized chemical mediator called cytokines. It also causes the activation of the
complement cascade to identify bacteria, activate or recruiting cells, and promote clearance
of antibody complexes or dead cells. Infectious agent is something that infiltrates another
living thing, like a human. When an infectious agent hitches a ride, our body have officially
become an infected host. Cells involved in the innate immune response are used to identify
infections by nonspecific chemicals generally shared by most pathogens termed PAMPs.
The first stage is to enable a cell to transport the infectious agent to the immune system,
and this is done in conditions conducive to an induction of an immune action, by activating
the immune system through a contagious agent which has defeated the innate antiinfectious defenses. APCs that express MHC-II molecules fulfil this job in the case of T
lymphocytes. A range of cells, including as tissue, B cells and dendritic cells, can serve as
APC. Those cells are adsorbing the infectious agent, ingesting part of the microbe ingested
and transforming it into small antigenic components. The resultant complex is carried to
the cytoplasmic membranes, thereby permitting activation of Th cells. These subunits are
linked to HLA intracellularly. APC's and T-lymphocytes expressed surface protein
interactions and APC-released cytokines are the costimulants of the Th cells. How antigen
is delivered to B-cells is not known, although the activation of the immune response in a
lymphoid organ has been thoroughly documented (lymph node, peri-intestinal lymphoid
tissues, spleen).
The lymphoid tissue has abundant opportunities for interaction with and collaboration
between those various cells, and all cellular factors essential for the inductive and efficient
phases for an immune response are present. Once encouraged to multiply and differentiate,
therapeutic cells can aid effector cell differentiation. But not all Th cells appear to be able
to support all kinds of effector cells. Activated Th1 cells produce cytokines, which work on
a range of cells, including macrophages (to further increase activation levels and increase
their capacity to remove intracellular infection agents) and cytotoxic T cells which are
extremely effective in eliminating virus-infected cells. The activated Th2 lymphocytes, by
contrast, segregate another cytokin group to support the proliferation and differentiation of
anti-stimulated B lymphocytes that subsequently develop into plasma cells. Plasma cells
synthesize huge quantities of antibodies.
The primary molecules for effectors in the humoral immune response are antibodies, as
described before. During activation of particular anticorps binding to a microbe and the
supplementary system, microorganisms are either consumed and destroyed with phagocytic
cells, or are killed by complementary lyse and ADCC mediated leukocytes. After removing
the micro-organism, the negative reaction mechanism is prominent and the immune
response is switched off.
A combination of several factors, such as the elimination of the positive stimulus
represented by the microorganism and the activation of immune regulation-based
lymphocytes which secretes cytokines that give inactivating signal to other lymphocytes,
seems to result in a downregulation of the immune reaction. A residual lymphocyte
population specific to the offending antigen will persist after the immune response. At the
end of this reaction. This is the memory cell population that is responsible for protection
following natural exposure or vaccination. The same generic cell sub-population can
trigger rapid rejection of numerous graft recipients. (702 words)
Question 2 (700 words)
Discuss the involvement of adaptive immunity, both cellular and humoral responses, due to
this infection
(10 marks)
Adaptive or acquired immune response lasts for days or weeks – far more than the innate
response; yet it is more pathogens-specific and has a more memory-based immunity.
Adaptive immunity is an immunity which arises when either a disease or vaccine is exposed
to an antigen. This component of the immune system is triggered when the innate response
to an infection is inadequate. Indeed, the adaptive response cannot be activated without
input from the innate immune system.
There are two different forms of adaptive reactions, the immuno-response of cells mediate
by T and the humoral immuno-response is regulated by activating B cell and antibodies. Tcells and B-cells that are specific to molecular pathogen structures are proliferating and
attacking the invading pathogen. Their assault may directly kill pathogen, or release
antibodies to improve pathogens' phagocytosis and disturb the infection. Adaptive immunity
also includes a memory that provides long-term reinfection protection for the hosts with the
same pathogen type and will allow an effective and rapid response when re-exposed to
them.
In the same way that humoral and cell-mediated responses are known now to be closely
interdependent, the distinction between specific and non-specific immune response to
infection has become hard to define. For example, natural killer (NK) cells and macrophages
play a role in innate immunity but they may be activated by lymphokines produced as a
result of a specific immune response. In addition, Fc receptor-bearing phagocytic cells may
act in an antigen-specific manner through binding antibody. When coated with specific
antibody, virus infected cells and other pathogens may be killed by antibody-dependent
cellular cytotoxicity (ADCC) mediated by macrophages and killer cells. If the inflammatory
response is unable to eliminate an invading organism, the stimulus persists long enough to
stimulate a specific immune response. The type of response that predominates is dependent
largely on the type of organism causing the infection. Often both T cell and antibody
responses are required to completely eliminate an invading pathogen.
Many of the bacteria that cause infectious illness in humans proliferate in the body's
surroundings, and the most intracellular pathogens transmit by extra-cellular fluids from
cells to cells. The extracellular gaps are protected by a human-induced immune response,
where B-cell antibodies kill extracellular micro-organisms and prevent intracellular disease
from spreading. Antigen triggers the activation of B cells and their distinction into plasma
cells that secrete antibodies. Helper T cell is commonly used to refer to a TH2 class of CD4
T cells. However, B cells may also be activated by a fraction of TH1 cells. The phrase
helper T cell means any CD4T cell that can activate a B cell with an armed effector. Helper
T cells also check the flipping of isotype and have a function in starting somatic hyper
muted genes in V-region antibodies.
Antigen binding to the B-cell antigen receptor activates B cells, and is internalized in
peptides which activate the T-helper cells at the same time. The immunity contributes to
three major methods in which antibodies attach to particular molecules onto the target cell
surface: cells, viruses and intracellular bacteria. This may be prevented and the disease is
neutralized by antibodies that attach to the pathogen. In order to prevent bacterial toxins
from entering cells, neutralization by antibodies is also necessary. The bacteria that
proliferate outside cells are protected against antibodies, largely by aiding pathogen
absorption by phagocytic cells specialized in destruction of ingested bacteria.
This is done in one of two ways by antibodies. On the first instance, Fc receptors in
phagocytic cells that bind to the C-region of the antibody are found to be bound antibodies
which cover the pathogen. The surface of a pathogen is termed opsonization for the purpose
of improving the phagocytosis. Alternatively, the proteins of the supplementary system
might be activated by antibodies binding to the pathogen surface. Complementary activation
causes complementary proteins to be attached to the pathogen surface by binding the
complementary receptors of phagocytes, which oppose the pathogen.
The other components of the supplement attract phagocytic cells at the infection site and
their terminal components can lysis of some bacteria directly through the formation of holes
in their membranes. The isotype or class of the anticorps generated determines the effector
mechanisms involved in a given reaction. (703 words)
End of Question
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