see https://www.goodreads.com/notes/234947136-all-about-allergies/114528832-mark-gerstein?ref=abp
+Part One: The Background
Highlight(yellow) – Chapter 2: The Immune System > Page 19 · Location 419
Cytokines are small proteins involved in the messaging between immune cells; they include interferons, tumor necrosis factor-alpha (TNF-α), and interleukins. As the name implies, interleukins are proteins that signal between white blood cells (WBCs); they are written in shorthand such as IL-4, IL-5, and IL-13. When cell signaling occurs, a ligand is released from a cell to find a receptor that is located either on the same cell or on another cell.
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We will go over some of these WBCs that are relevant to this book. For the innate immune system, neutrophils destroy bacteria and fungi by eating them, through the process called phagocytosis. As noted in chapter 1, cells that can cause phagocytosis are known as phagocytes, which also include monocytes, macrophages, and dendritic cells. Macrophages and dendritic cells are examples of antigen-presenting cells (APCs) because they capture antigens and then show them to the adaptive immune system. Eosinophils attack parasites and release various chemical mediators that may lead to allergic reactions and inflammation.
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They are also located near blood vessels and nerves. Mast cells hold granules that store various chemicals and are released during a process called degranulation. These cells can be activated for many reasons that will be discussed throughout many chapters of this book. A couple of triggers of mast cell activation worth mentioning now are physical trauma and emotional stress. The chemical that most people are familiar with is histamine, which can cause blood vessel widening (vasodilation), itching, urticaria (hives), angioedema (swelling), and airways becoming smaller due to smooth muscle contraction (bronchoconstriction). In the gastrointestinal tract, histamine stimulates stomach acid production.
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When immune complexes are not cleared effectively, they can deposit in tissues such as joints, blood vessels, or kidneys, which leads to inflammation. Another way to think about immune complexes is as airport luggage. The antigens are luggage bags, while the antibodies are the luggage tags, and the immune complexes form when you have labeled luggage. The complement system and phagocytes are the airport crew that pick up the labeled luggage and remove it from the plane. If there are too many labeled bags or too few workers, then the luggage may pile up before reaching baggage claim.
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B cells are produced in the bone marrow (hence the name B cells) and eventually turn into two main cell types: memory B cells and plasma cells. Memory B cells help remember a specific pathogen after an initial infection or vaccination; they lie dormant in the body for many years and rapidly respond if the pathogen returns. Plasma cells produce large amounts of antibodies during an active infection. They can be short-lived during an infection or long-lived to continuously produce antibodies from the bone marrow to maintain long-term immunity. B cells can also act as APCs (antigen-presenting cells) by ingesting pathogens and presenting them to T cells.
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T cells are produced in the bone marrow and mature in the thymus (hence the name T cells) and have a variety of functions and subtypes. Helper T cells (CD4 + T cells) activate other immune cells to coordinate an immune response. Cytotoxic, or killer T cells (CD8 + T cells), destroy infected or cancerous cells. Regulatory T cells (Tregs) help promote immune tolerance and prevent autoimmune reactions.
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Before moving on, I want to pay special attention to a subtype of helper T cells called T-helper type 2 (Th2) cells because they play a pivotal role in the development of allergic reactions. These cells release IL-4 and IL-13, which are cytokines that cause B cells to produce IgE antibodies. IL-13 also causes mucus production and airway hyperresponsiveness in people living with asthma. Th2 cells also release IL-5, which promotes the activation, recruitment, and survival of eosinophils, which are cells that contribute to inflammation.
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During sensitization, APCs such as dendritic cells capture the allergen and present it to a naive T helper cell. Those T cells turn into Th2 cells and influence B cells to produce IgE antibodies that can specifically bind to the allergen. These antibodies then bind to IgE receptors called FcεRI, which are located on the surface of mast cells and basophils. Once this happens, you are considered sensitized to the allergen. If the immune system sees the allergen in the future, then the allergen may bind to the specific IgE antibodies on the mast cells or basophils in a process called cross-linking. This leads to degranulation, which releases various chemical mediators that we mentioned previously. The symptoms of a type I hypersensitivity reaction vary depending on the site and extent of mast cell and basophil activation. Symptoms usually occur within a few minutes to an hour of exposure and may include sneezing, nasal congestion, runny nose (rhinorrhea), wheezing, shortness of breath, urticaria, angioedema, eczema, or the potentially life-threatening systemic reaction, anaphylaxis.
Highlight(yellow) – Chapter 3: The Anatomy of Allergies > Page 31 · Location 592
The bone marrow is the soft, spongy tissue inside bone where blood cells are created (i.e., hematopoiesis). It is broadly categorized into two types: red marrow and yellow marrow. Red bone marrow is mostly found in flat bones such as the sternum, ribs, and skull as well as the ends of long bones such as the femur and humerus. There is more red marrow in children than in adults. This is the area of bone marrow that produces red blood cells, white blood cells, and platelets. As people age, some red marrow is replaced by yellow marrow, which is found in the hollow center of long bones.
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A type of dendritic cells in the epidermis called Langerhans cells plays a crucial role in initiating allergic reactions in the skin. These cells capture antigens and travel to local lymph nodes to activate T cells, which starts the adaptive immune response. T cells also found in the skin are known as resident memory T cells because they respond quickly to previously encountered pathogens. B cells and plasma cells are present in the skin to produce antibodies that neutralize pathogens. The immune system in your skin also interacts with nerve cells and
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Secondary skin lesions are changes that occur in primary skin lesions due to external factors such as scratching or the natural progression of a disease. Examples include crusts, scales, erosions, ulcers, fissures, atrophy, and lichenification. Crusts are dried blood or pus on the surface of the skin; they are often seen after vesicles or pustules have ruptured. Scales are flakes of dead epidermal cells, which are usually due to accumulation of keratin or abnormal skin shedding. Erosions are shallow losses of epidermis that heal without scarring. These are often seen after a vesicle or bullae rupture. Ulcers are deeper losses of skin than erosions but may still heal without scarring. Fissures are cracks in the skin that may extend into the dermis, which is often seen with eczema. Atrophy is thinning of the skin, while lichenification means the skin has thickened.
Part Two: Allergic Diseases
Highlight(yellow) – Chapter 8: Eczema > Page 109 · Location 1692
The immune system in the skin functions differently in people living with eczema. It is often referred to as “type 2 inflammation” because of a specific type of T cell, Th2. These cells are activated by various substances called alarmins. Th2 cells release cytokines IL-4 and IL-13, which promote further inflammation and lead to B cells producing IgE antibodies. It is unclear whether this inflammation is triggered by the faulty skin barrier function or by the skewed immune response.
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Topical steroids are the medications most used to treat eczema. They help reduce the release of various chemicals that promote inflammation. Examples include hydrocortisone, triamcinolone, mometasone, desonide, and clobetasol. The strength of the medication depends on its concentration and the steroid agent itself. For example, clobetasol propionate 0.05 percent is much stronger than hydrocortisone 2.5 percent. While these medications are usually well tolerated, there are some potential side effects to be aware of. Long-term use of topical steroids may cause the skin to thin, appear lighter, erupt a new rash that looks like acne, or become allergic to the medication itself.
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There are several nonsteroidal topical medications that may be prescribed. Protopic (tacrolimus) and Elidel (pimecrolimus), called calcineurin inhibitors, do not cause skin atrophy or other problems that are caused by steroids. However, these medications can cause a temporary burning or stinging sensation when applied to the skin. There is also a black box warning from the FDA about a theoretical concern regarding a potential link between these medications and cancer. Multiple long-term studies have disproven this link, and the boxed warning was removed in Canada, but it is still present in the United States.
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Over the past few years, a newer class of medications has been released to treat eczema and it comes in both oral and topical preparations. These medications block the enzyme Janus kinase (JAK), which is involved in the inflammation that creates eczema. They may relieve eczema faster than other medications, but they can cause broader immune-system suppression. There was a large, randomized safety study of older patients who had multiple medical problems, including rheumatoid arthritis and cardiovascular disease, and were taking the JAK inhibitor tofacitinib. The study authors reported that people taking tofacitinib may have an increased risk of serious infections, heart attack, stroke, cancer, blood clots, and even death. The FDA put a black box warning on these medications to alert people to this potential risk. However, multiple meta-analyses, including dozens of clinical trials of JAK inhibitors for treating eczema, did not report these increased risks.
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Contact dermatitis is an inflammatory skin disease that occurs when the skin comes into direct or indirect contact with substances. This disease has multiple subtypes and multiple underlying mechanisms. There are roughly 85,000 human-made chemicals, and roughly 2,800 have been identified as contact allergens. One of the challenges with contact dermatitis is that it can look a lot like other skin diseases, such as eczema. If you suspect that you may have contact dermatitis, an allergist or dermatologist may be able to help you. Contact dermatitis is usually divided into irritant contact dermatitis and allergic contact dermatitis. Irritant contact dermatitis, estimated to account for 80 percent of cases of contact dermatitis, is the result of direct tissue damage from irritating substances, as with a typical diaper rash. Allergic contact dermatitis is a delayed allergic reaction that can be caused by substances such as poison ivy and nickel.
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The rash usually appears red, itchy, and scaly and may have bumps. Sometimes, there may be blisters, swelling, burning, and warmth. The rash is usually located where the skin is in contact with the allergen, but the allergen can be transferred to another part of the body by touch. Common areas affected include the hands, scalp, face, and eyelids.
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When there is a rash, topical medications may be needed. Usually, a prescription for a topical steroid or calcineurin inhibitor is needed to decrease the immune response. Stronger steroids are typically avoided on the face because of potential side effects, including an eruption of acne, additional hair growth, thinning of the skin, and pigment changes. If symptoms are severe, an oral steroid or other immunosuppressant medications may be prescribed. There is a common misconception about treating contact dermatitis, which I will illustrate with another story.
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