The Immune System

The immune system is necessary for human survival in the vast environment full of pathogens. It is crucial in fighting off pathogens, such as viruses and bacteria that often cause infections. It comprises various immune cells that together work to mount an immunological response against invaders.

Running head: IMMUNE SYSTEM 1
The Immune System
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IMMUNE SYSTEM 2
The Immune System
The immune system is necessary for human survival in the vast environment full of
pathogens. The human body would be susceptible to infectious diseases in the absence of an
immune system. It is crucial in fighting off pathogens, such as viruses and bacteria that often
cause infections. It comprises various immune cells that together work to mount an
immunological response against invaders. Notably, the innate (non-specific) and adaptive
(acquired) immune systems scavenge dead cells, destroy malignant cells, and protect the body
from pathogens via various mechanisms. Not only does the immune system fight infections but
also crucial in mounting immunological effects during healing processes.
Types of Immune Systems
Innate (Non-specific) Immunity
Innate immunity is quick and effective. A person inherits the non-specific immunity from
parents. Its non-specificity is elicited from its response against various invaders. Innate immunity
serves as a barrier to the entry of pathogens via the external and internal surfaces. For instance, it
destroys within a short period the bacteria that tries to enter the skin through a wound. The
natural immunity comprises of the skin, mucosal lining, leukocytes, and other components of
body fluids. The skin and mucosal lining offer protection from the outside. They act as
mechanical barriers; hence, preventing the entry of invaders (Thompson, 2015). More also,
saliva and tears have lysozyme that elicits digestive properties which render antigens mild.
Additionally, the movements by cilia and gastrointestinal muscles prevent the adherence of
pathogens to membranes. The mucosal lining secretes mucus that traps and immobilizes
pathogens. Besides, the human body temperature and vaginal secretions create an unfavorable
environment for microbes to thrive.

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However, the passage of pathogens through the physical barriers trigger the second line
of defense mechanisms. It recruits cells to the site of infection. Typically, the hematopoietic stem
cells differentiate into myeloid progenitor cells that synthesize various leucocytes, for instance,
macrophages, monocytes, neutrophils, natural killer cells, dendritic cells, eosinophils, and
basophils. Notably, phagocytic leucocytes have pattern recognition receptors (PRRs) which
recognizes particular pathogen-associated molecular patterns (PAMPs) (Plato, Hardison &
Gordon, 2015). If invaders enter the body, dendritic cells present on the skin and lymph nodes
ingest and process the exogenous antigens for easier presentation to T-lymphocytes by Major
Histocompatibility Complex (MHC) II (Nicholson, 2016). Also, innate immune systems release
natural killer cells that adhere to viruses and secrete cytokines that lyse viral components.
Besides, the freely circulating eosinophils adhere, poke holes, and ingest pathogens that
are too large for other phagocytes to digest. According to Iwasaki and Medzhitov (2015), the
innate immune system elicits its response by phagocytosis; pathogens adhere to the phagocytic
cells whose membranes extend to surround the invader. The phagocytes take the microbe into a
vesicle with lysosomes that process the pathogens into antigenic fragments, which are presented
to T-lymphocytes. Activated T-lymphocytes trigger the release of cytokines and interleukin 2
that destroy the antigens. More also, it activates the complement system; it comprises of several
proteins that work to eliminate infectious pathogens (Merle et al., 2015). The system marks
invaders; attract phagocytic cells; dissolve bacterial cell walls; lyse viruses. As a result,
inflammation ensues due to infiltration of phagocytes into the site of invasion. Inflammatory
response results in redness, pain, and fever (Vincenzo et al., 2015).
Adaptive (Acquired) Immunity

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After an unsuccessful action of the innate immunity, the adaptive or acquired immune
system sets in. According to Iwasaki and Medzhitov (2015), adaptive immunity starts in about a
week after the body’s initial encounter with pathogens. It is more specific; it accurately targets
invaders and their antigens. The adaptive immunity is crucial in the fight against infections due
its immunological memory: it remembers and acts against specific antigens. Antigens are foreign
molecules that induce immune responses. Endogenous antigens arise from previously healthy
cells due to viral attacks or metabolism. Besides, exogenous antigens enter the body through
various routes, such as inhalation, injection, or ingestion. Tumor antigens, on the other hand, are
released from tumor cells. Also, autoimmunity is responsible for the production of autoantigens.
The adaptive immune system is more effective than innate immunity. The presence of
already known antigenic components triggers quick responses. Besides, the adaptive immune
system generates memory cells that are specific to antigens encountered in primary responses.
Memory cells live longer; a property that makes the adaptive immune system to respond faster
after secondary exposure to a similar antigen (Nicholson, 2016). Adaptive immunity reacts
through various mechanisms: the humoral and cell-mediated mechanisms. Antibodies, the
proteins generated in response to antigens, fight pathogens in blood and body fluids.
Alternatively, cell-mediated immunity is crucial in eliminating pathogens within tissues.
The B and T-lymphocytes are the crucial cells that make up the adaptive immunity. B-
cells are the primary component that builds up the humoral immune system. They produce
antibodies that specialize against a particular antigen (Marshall et al., 2018). However, B-
lymphocytes produce antibodies when they are activated fully. The antibodies serve various
purposes: activating the complement system, neutralizing antigens, and initiating phagocytosis.
When B-cells encounter their cognitive antigens and receive signals from T-helper cells, they

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mature into plasma and memory B cells (Hoffman, Lakkis & Chalasani, 2015). Plasma B-cells
secrete copious amounts of antibodies that help to destroy the microbes by adhering to them and
activating the complement system. They are short-lived; they undergo programmed death when
an immunological response is complete. Notably, the B-cells may become activated in the
presence or absence of T-cells (Hoffman, Lakkis & Chalasani, 2015. T-cell dependent
activations trigger a humoral response in organisms with T-cells.
T-lymphocytes are essential in cell-mediated immunity and mature in the thymus. About
80-90 % circulate in the blood and thoracic ducts respectively. T-cell receptors distinguish these
lymphocytes from B-cells. The various types of T-lymphocytes are T-helper, T-cytotoxic, and
memory T-cells. T-helper trigger the maturation of B-cells into plasma cells (Jain & Pasare,
2017). Also, they activate cytotoxic T cells. The delivery of antigenic components by MHC II
activates the T-cells, which divides to produce cytokines that regulate the immune response to
pathogens (Jain & Pasare, 2017). By contrast, the cytotoxic T cells express CD8+glycoproteins
and T-cell receptors on their surfaces, which are specific to MHC 1 present on infected cells.
Thus, they secrete cytokines, and interferon destroy virus or tumor infected tissues.
Immune Response to Infections
The interaction between pathogens and body cells trigger immunological responses.
Physiological barriers give innate protection. The skin, mucosal membranes, and body secretions
prevent the entry of pathogens. However, the penetration of invaders past these barriers triggers
the second line of defense (Nicholson, 2016). Phagocytes through endocytosis, pinocytosis, and
phagocytosis take in the invaders. It triggers an inflammation of the affected sites that release
histamine while increasing blood supply to the region. The histamines cause infiltration of the
blood vessels that release basophils and clotting factors to the site of infection (Nicholson, 2016).

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Lysosomes fuse with the phagocytes to facilitate the degradation of antigens. Antigen debris is
then removed via exocytosis. Alternatively, smaller fragments are packaged and presented to T
and B-cells by MHC complexes. The activation of adaptive immunity triggers the differentiation
of B cells into plasma cells that release antibodies to fight infections (Thompson, 2015). The T
lymphocytes may differentiate into T-helper and T-cytotoxic cells. Notably, the T-helper cells
facilitate the maturation of B-cells that regulate active immune responses against infections.
The Healing Process
A patient’s healing process is crucial and heavily relies on the immune cells. At first, the
blood platelets aggregate at the site of infection to initiate the clotting cascade. It is the
homeostatic phase that prevents the loss of blood while creating a barrier from the external
environment (Laruoche et al., 2018) The clotting cascade also triggers the release of immune
cells to the affected area, which initiates the inflammatory phase. Thus, the site of infection
swells and becomes red due to dilation of blood vessels that facilitate the movement of immune
cells. Neutrophils and monocytes are the first responders; the monocytes differentiate into
macrophages that initiate the wound healing process (Julier et al., 2017). Macrophages digest
antigen debris at the infection sites. Besides, they promote the growth of biological scaffold
tissues around sites. Also, macrophages promote the production of fibroblast growth factors that
repair the damaged extracellular matrix. Fibroblasts differentiate into myofibroblasts that
contract allowing the closure of wounds (Strbo, Yin & Stojadinovic, 2018). Besides,
macrophages trigger angiogenesis; they secrete Vascular Endothelial Growth Factor (VEGF) that
facilitate the formation of injured blood vessels. The last phase of the healing process involves
tissue remodeling (Julier et al., 2017). At this point, the macrophages die to allow the
strengthening of the tissues and muscles.

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In conclusion, the immune system is essential in eliminating pathogens as well as in
promoting a patient’s healing process. The immune system comprises of innate and adaptive
immune responses. Pathogens encounter the first line of defense, which is a significant
component of innate immunity. At this phase, the skin and mucosal membranes form a barrier
that prevents the entry of invaders. More also, body secretions and temperature create
unfavorable thriving environments for these microbes. However, pathogen penetration through
mechanical barriers triggers adaptive immunity whose primary components are the B and T-
lymphocytes. B- lymphocytes produce antibodies against antigens. Besides, they differentiate
into plasma and memory B-cells. Nonetheless, the T-lymphocytes differentiate into T-helper
cells that trigger the maturation of B-cells and activation of T-cytotoxic cells. Also, wound
healing processes rely on the action of immune cells such as macrophages. They release
fibroblasts and Vascular Endothelial Growth Factor (VEGF) that trigger the regeneration of new
tissues and blood vessels.
References
Hoffman, W., Lakkis, F. G., & Chalasani, G. (2015). B Cells, antibodies, and more. Clinical
journal of the American Society of Nephrology : CJASN, 11(1), 137-154.
doi:10.2215/CJN.09430915

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Iwasaki, A., & Medzhitov, R. (2015). Control of adaptive immunity by the innate immune
system. Nature immunology, 16(4), 343.
Jain, A., & Pasare, C. (2017). Innate control of adaptive immunity: Beyond the three-signal
paradigm. Journal of immunology, 198(10), 3791-3800. doi:10.4049/jimmunol.1602000
Julier, Z., Park, A. J., Briquez, P. S., & Martino, M. M. (2017). Promoting tissue regeneration by
modulating the immune system. Acta Biomaterialia, 53, 13-28.
Laruoche, J., Sheoran, S., Maruyama, K., & Martino, M. M. (2018). Immune regulation of skin
wound healing: Mechanisms and novel therapeutic targets. Advances in wound care, 7(7),
209-231. doi:10.1089/wound.2017.0761
Marshall, J. S., Warrington, R., Watson, W., & Kim, H. L. (2018). An introduction to
immunology and immunopathology. Allergy, asthma, and clinical immunology : official
journal of the Canadian Society of Allergy and Clinical Immunology, 14, 49.
doi:10.1186/s13223-018-0278-1
Merle, N. S., Noe, R., Halbwachs-Mecarelli, L., Fremeaux-Bacchi, V., & Roumenina, L. T.
(2015). Complement system part II: role in immunity. Frontiers in immunology, 6, 257.
Nicholson, L. B. (2016). The immne system. Essays in biochemistry, 60(3), 275-301.
doi:10.1042/EBC20160017
Plato, A., Hardison, S. E., & Brown, G. D. (2015). Pattern recognition receptors in antifungal
immunity. Seminars in immunopathology, 37(2), 97-106.
Strbo, N., Yin, N., & Stojadinovic, O. (2014). Innate and Adaptive Immune Responses in Wound
Epithelialization. Advances in wound care, 3(7), 492-501. doi:10.1089/wound.2012.0435
Thompson, A. E. (2015). The immune system. JAMA, 313(16), 1686.
doi:10.1001/jama.2015.2940

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Vincenzo, B., Asif, I. J., Nikolaos, P., & Francesco, M. (2015). Adaptive immunity and
inflammation. Intearnational journal of inflammation, 1. doi:10.1155/2015/575406