Hypersensitivity and Allergic Fungal Manifestations: Diagnostic Approaches
Johan A. Maertens, Kieren A. Marr in Diagnosis of Fungal Infections, 2007
Exposure to fungal antigens can elicit both humoral and cellular immune responses. Humoral response to allergenic fungi is polyclonal in nature and is characterized by type I and type III hypersensitivity reactions. Type 1 (immediate) hypersensitivity reaction involves the release of mediators from mast cells or basophils caused by the bridging of IgE antibodies on the surface of these cells. Clinical manifestations of this type of reaction include rhinitis and asthma. Type III hypersensitivity (immune complex-mediated) owes its origin to formation of large quantities of soluble antigen-antibody complexes in the blood. These antigen-antibody complexes lodge in the capillaries between the endothelial cells and the basement membrane. The antigen-antibody complexes activate the classical complement pathway and complement proteins and attract leukocytes to the area. The leukocytes then discharge their killing agentsand promote massive inflammation. This leads to tissue death and hemorrhage. Clinical manifestations of this type of reaction include allergic bronchopulmonary aspergillosis (ABPA) with extensive pulmonary tissue damage.
Hypersensitivity
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
A type III hypersensitivity (Figure 58.3) is an immune-complex-mediated reaction resulting in the deposition of antigen–antibody complexes in host tissues, leading to complement activation, neutrophil infiltration and tissue damage. There are two forms of reaction: (i) complexes formed in the circulation and then deposited in the tissues, causing systemic effects (e.g. serum sickness) and (ii) complexes formed within the tissues resulting in localized effects (e.g. Arthus phenomenon). Normally, immune complexes deposited in small amounts in tissues are easily removed by the reticuloendothelial system, but in type III hypersensitivity, these immune complexes are either too abundant or too small to be cleared effectively.
SBA Answers and Explanations
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury in SBAs for the MRCS Part A, 2018
Type III hypersensitivity reaction occurs when there is accumulation of immune complexes (antigen-antibody complexes) that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and activation of leukocytes. Such reactions result in immune complex diseases. Antibody (IgG) binds to soluble antigen, forming a circulating immune complex. Examples include systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).
An unusually “complex” glomerulonephritis
Published in Baylor University Medical Center Proceedings, 2022
Gabriela Martinez-Zayas, Daniel Savino, Sumit Kumar, Kathryn H. Dao
Hypersensitivity reactions are inappropriate immune responses to an antigen and are classified into four types, I to IV.1 Type III hypersensitivity reactions or immune-complex (IC) reactions occur when excess antigen-antibody complexes cannot be cleared and precipitate in tissues.2,3 If deposited in the renal glomeruli, immune complexes can cause glomerulonephritis (GN). Common associations with IC-GN include infections (e.g., HIV), autoimmune diseases (e.g., systemic lupus erythematous), and vaccines (e.g., pneumococcal).2,3 Vaccines enhance host defenses through immune activation against antigen, with some inducing IC formation important in B, T, and antigen-presenting cell activation.4 Amid the pandemic, SARS-CoV-2 infection has been reported to cause IC diseases including GN,5,6 and COVID-19 vaccines may induce de novo autoimmunity or flare underlying immune-mediated inflammatory diseases.7–9 Here, we present an unusual case of IC-GN presenting shortly after COVID-19 vaccination in a patient with granulomatosis with polyangiitis (GPA) and HIV infection.
Understanding Retinal Vasculitis Associated with Brolucizumab: Complex Pathophysiology or Occam’s Razor?
Published in Ocular Immunology and Inflammation, 2022
Ashish Sharma, Nilesh Kumar, Nikulaa Parachuri, Sonali Singh, Francesco Bandello, Carl D. Regillo, David Boyer, Quan Dong Nguyen
It is possible that small size may allow higher molar concentration and incite a strong local immune reaction leading to inflammation. We have highlighted the role of type III hypersensitivity reaction (HSR) in the past.15 The majority of vasculitic diseases involve the deposition of antigen-antibody complex, which is Type III HSR. These deposits have been shown in the capillary bed and vessel walls and can lead to occlusive vasculitis. Arthus reaction, a subtype of Type III HSR has been reported in patients on systemic monoclonal antibody (mAb), including systemic anti-VEGF therapies. Such reactions are assumed to be due to high antigen load, which leads to a subsequent increase of antibodies.16,17 Arthus reaction is more frequent in patients with auto-immune conditions. The higher molar concentration of brolucizumab (11 and 22 times greater than aflibercept and ranibizumab, respectively), if antigenic, may produce a higher rate of antibody formation. Type III HSR is due to the formation of biologic/ADA immune complexes in the circulation. When these complexes are in the correct stoichiometric ratio, they are deposited in tissues and cause inflammation and tissue damage. The requirement of the correct ratio to have tissue deposition might explain why vasculitis is seen in some individual rather than in clusters as each individual having differing amounts of ADAs leading to different stoichiometric ratios.18
The dilemma: scleroderma renal crisis vs lupus nephritis in a patient with mixed connective tissue disorder
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Nicola Jackson, Shion Betty, James Appiah-Pippim, Yolin Bueno, Sana Makhdumi
Renal complications occur in approximately 25% of patients with MCTD[8]. The pathogenesis of scleroderma renal crisis (SRC) is not well understood[9]. It is thought to be related damage to the endothelial of the renal vasculature, along with activation of the renin-angiotensin-aldosterone system[9]. While lupus nephritis is the result of a type-III hypersensitivity reaction[10]. Both lupus nephritis and SRC can present with proteinuria and hematuria [9,10]. However, lupus nephritis can also present with polyuria, nocturia, and foamy urine[10]. On the other hand, SRC presents with moderate to severe hypertension associated with oligo-anuric acute renal failure[9].
Related Knowledge Centers
- Antibody
- Classical Complement Pathway
- Clearance
- Immune Complex
- Inflammation
- Malaria
- White Blood Cell
- Hypersensitivity
- Antigen
- Subacute Bacterial Endocarditis