Personal Narrative: The Innate Immune System

When I was a young girl I remember playing in the woods with my brother and sister. We accidentally disturbed a hive of angry bees, and we each got stung five to ten times. We all were crying and screaming as we were being chased back up to our cabin. Halfway up the hill by sister fell down because her throat started to close up. My mom fortunately heard us yelling and ran down to my sister with an Epi-pen. The bees were still chasing us, so after my mom stabbed my sister with the Epi-pen she picked her up and we all ran into the cabin. My brother and I got stung about fifteen times and only had the little red bumps to show for it. My sister on the other hand, got stung about twenty times and almost died. I was so confused as to why. I asked

my mom why my throat didn’t close up too and my mom, still in a panic, told me that my sister has allergies and I don’t. Being the curious kid I was, I then asked my mom why I didn’t have allergies. She didn’t really have an answer for me.
A few years later my brother and I both came down with strep throat at the same time. We were both prescribed antibiotics and my brother quickly recovered. However, I didn’t. I remember sitting in the emergency room when they told me I needed a tonsillectomy. I had no idea what that was, but I was happy when they said I could eat all the ice cream in the world afterwards. I was confused as to why my brother got better and I didn’t. If we both had strep throat, how come our bodies reacted differently?
This is a question that has baffled scientists for hundreds of years. There is still much to learn about our immune system because there is a uniqueness in how our immune systems work that varies from person to person. In order to discuss the individuality of our immune system, it is first important to discuss how our immune systems work.
The immune system is broken down into two parts, the innate immune system and the adaptive immune system. The innate immune system is our natural immunity, or our ability to resist infection by means of normally present body functions. In other words, the innate immune system is nonspecific, and it is the same for all pathogens or foreign substances that we are exposed too. The adaptive immune system is characterized by specificity for each individual pathogen or foreign substance that we are exposed to and the ability to remember past exposure. The memory and specificity result in an increased efficiency and response to a pathogen upon repeated exposure, something that the innate immune system can’t do. Both systems work with one another and are necessary for an overall healthy immune system.
There are many cells in both the innate and adaptive immune systems that work with one another in order to protect our bodies against pathogens.

Cells in the innate immune system include neutrophils, eosinophils, basophils, monocytes, macrophages, mast cells, and dendtritic cells. Neutrophils quickly reach the site of infection to phagocytose and kill invading organisms. Eosinophils release granules to kill parasitic worms and are also involved in allergic reactions. Basophils and mast cells mediate allergic reactions by releasing granules containing substances that cause blood vessel dilation, airway constriction, and recruitment of more cells. Monocytes and macrophages phagocytose pathogens and foreign particles, kill pathogens and tumor cells, remove old red blood cells from circulation, secrete substances that activate other cells (cytokines), and activate the immune system. Dendritic cells are phagocytic and also effective at antigen

presentation.
Cells in the adaptive immune system include B and T lymphocytes and natural killer cells. B cells make antibodies, while T cells recognize specific antigens, kill virally-infected or cancerous cells, and activate or suppress other immunological cells. Natural killer cells don’t recognize specific antigens, but destroy cells that lack certain surface proteins that might be virally-infected of cancerous.
The two cells that I am going to focus on are B and T lymphocytes. Both types of cells go through an extensive “education” before they can fight pathogens. B cells remain in the bone marrow, while T cells move to the thymus for maturation. During their education, these cells must pass two quality-control steps. The first step ensures that each cell is capable of making a response if they encounter their particular invader, making sure that no further energy is wasted on keeping non-responsive cells alive, or expanding these cell populations. The second step ensures the cells won’t respond against the host’s body, a process called negative selection. Any cell that does respond to self-antigens must be removed so it doesn’t cause damage. Failure to remove these self-reactive cells can result in autoimmune diseases.
Broadly speaking, T cells can be divided into two different types, cytotoxic T cells and T helper cells. T helper cells, or CD4 T cells, bind an epitope consisting of an antigen fragment lying in the groove of a class II major histocompatibility molecule. They are essential for cell-mediated and antibody-mediated branches of the immune system. T helper cells bind to antigens presented by antigen-presenting cells like macrophages and dendritic cells. The T cells then releases lymphokines that attract other cells to the area resulting in inflammation. T helper cells also bind to antigens presented by B cells, resulting in the secretion of antibodies against the pathogen.
Cytotoxic T cells, or CD8 T cells, secrete molecules that destroy the cell to which they have bound via the class I major histocompatibility molecule. This can prevent a virally infected cell from releasing a fresh crop of viruses by killing the infected cell.
B cell receptors, found on the surface of B cells, bind intact antigens, whether if they were soluble in plasma or from the surface of antigen-presenting cells like macrophages or dendritic cells. After the B cell engulfs the antigen molecules, the antigen is digested into fragments and then displayed on the surface of the cell via the class II major histocompatibility molecule. Helper T cells that are specific for the antigen, then binds to the B cells allowing secretion of lymphokines that stimulate the B cell to proliferate and differentiate into plasma cells that secrete soluble B cell receptors, or antibodies.
This crude background into how our immune systems work allows us to discuss the individuality of our immune systems. For the most part, our immune systems work in the same way. The main goal is to protect our bodies against harmful foreign pathogens. However, in many instances this can go wrong. Examples include autoimmunity and hypersensitivity.
Autoimmune diseases are disorders in which immune responses are targeted toward self-antigens and result in damage to organs or tissues themselves. In other words, a person’s body is attacking itself. Normally, our immune system is able to differentiate between self and non-self antigens, so that self-antigens are not destroyed. This conditioning happens during B cell and T cell maturation in the bone marrow and thymus. When self-reactive cells escape negative selection and apoptosis, an autoimmune disease can develop.
Autoimmune disorders include systemic and organ-specific autoimmunity. Examples of systemic autoimmune disorders are systemic lupus erythematosus, rheumatoid arthritis, and granulomatosis with polyangiitis. Examples of organ-specific autoimmune disorders include Addison’s disease, autoimmune hemolytic anemia, celiac disease, multiple sclerosis, and type I diabetes mellitus.
Hypersensitivity is an exaggerated response to a typically harmless antigen that results in injury to the tissue, disease, or even death. Hypersensitivity can be classified into four different types; type I, type II, type III, and type IV.
Type I hypersensitivity is commonly thought of as allergies.

It is why my sister almost died of a bee sting that just left a simple red bump on me. It involves production of IgE antibody to the inducing antigen or allergen. Type II hypersensitivity is known as antibody-mediated cytotoxic hypersensitivity. Examples include transfusion reactions, hemolytic disease of the newborn, and autoimmune hemolytic anemia. It involves the production of IgG or IgM antibodies to antigens on the surface of host cells. These antibodies can destroy the cells through complement-mediated cytolysis, opsonization and phagocytosis, or antibody-dependent cellular cytotoxicity. Type III hypersensitivity involves formation of IgG or IgM antibody that reacts with soluble antigen under conditions of slight antigen excess to form small complexes that precipitates in the tissues. Examples of type III hypersensitivity include serum sickness, lupus erythematosus, and rheumatoid arthritis. Type IV hypersensitivity is a cell-mediated or delayed type of hypersensitivity. Examples include contact dermatitis and hypersensitivity

pneumonitis.
The big question needed to be answered is why do some people develop autoimmune disorders or a hypersensitivity and others do not? How and why are our immune systems acting differently? These questions spark the whole nature versus nurture debate. Are some people genetically inclined to develop an immune disorder, or are they raised in an environment that promotes the development of one? Many scientists want a clean answer to this question, but the best answer they can give us is that it is probably a mixture of genetics and the environment we are in.
There are many genetic factors that play a role in the development of an autoimmune disease. For example, autoimmune diseases are often more prevalent among family members than among unrelated individuals and are more prevalent among identical than non-identical twins or siblings. Researchers conducting molecular studies are continuing to identify specific genetic mutations that are associated with autoimmune diseases. Examples include the HLA-B27 allele and the development of ankylosing spondylitis, an autoinflammatory disorder that affects the spine.