Constitutive Host Resistance
Julius P. Kreier in Infection, Resistance, and Immunity, 2022
Antibodies are components of the inducible immune response and will be considered fully in chapter 7. The complement system is involved in both the constitutive and the inducible systems. The complement system is a group of serum proteins which activate each other sequentially following activation of the initial component by contact with permissible surfaces of microbes or other foreign material, or by contact with immune complexes in the body. When involved in the constitutive defense, complement is activated through the alternate pathway. When involved in the inducible response, activation is through the classical pathway. In the latter case, combination of antibody with the microbe or other target initiates activation of CI; in the former, direct binding of the constitutive serum protein—the complement component C3—with the microbe or other target initiates the process (Figure 3.5).
Immune system and Innate Immunity
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The functions of the components of complement include: Anti-infective functions. (i) Opsonization (coating the walls of bacteria so that they can attract and bind to phagocytic cells and be easily ingested; (ii) chemotaxis; (iii) activation of neutrophils and mononuclear phagocytes and (iv) lysis of bacteria or foreign cells (Figure 55.1).Interplay between innate and adaptive immune systems. Immunomodulation of B-cell responses to specific antigen by binding to complement receptors on the B-cell surface, resulting in enhancement of antibody responses and immunological memory.Clearance. Clearance of (i) immune complexes and (ii) apoptotic cells via C1q, C3 and C4.
Combining Evidence Over Multiple Individual Analyses
Rens van de Schoot, Milica Miočević in Small Sample Size Solutions, 2020
Van der Ham et al. (2019) were not interested in testing the null hypothesis as shown in Equation 9.4. Rather, they had formulated three informative hypotheses about the population regression coefficients. These hypotheses are presented in the left column of Table 9.1. specifies the expectation that that there is no effect of condition, while valance and arousal have a positive effect on relative time estimation, while describes the expectation that all regression coefficients are positive. Finally, is the complement of and specifies the expectation that at least one of the regression coefficients for arousal and valence is not positive or that the effect of condition is different from zero. The equivalent of these average hypotheses was considered at the individual level. These individual hypotheses are presented in the right column of Table 9.1. The only difference with the population level hypotheses is that the hypotheses now concern individual regression coefficients rather than population regression coefficients.
Involvement of the complement system in immune thrombocytopenia: review of the literature
Published in Immunological Medicine, 2023
Risa Shindo, Ryohei Abe, Kenji Oku, Tomoki Tanaka, Yu Matsueda, Tatsuhiko Wada, Yoshiyuki Arinuma, Sumiaki Tanaka, Tatsuyoshi Ikenoue, Yoshitaka Miyakawa, Kunihiro Yamaoka
The complement system comprises a group of proteins responsible for innate immunity, which are activated sequentially following specific triggers resulting in opsonization, local inflammation, and cell membrane destruction. The complement system is involved in a variety of systemic manifestations of some autoimmune diseases, such as SLE and APS. In particular, activation of the classical complement pathway by immune complexes, and subsequent amplification by the alternative pathway, leads to local inflammation and, ultimately, tissue damage through the production of membrane attack complex (MAC, C5b-9) (Figure 2). A recent phase I trial of sutimlimab, an antibody against C1s approved for cold agglutinin disease, showed favorable results in a limited number of pITP patients [8]. Hypocomplementemia is a frequent complication of SLE, but has also been reported to be associated with hypocomplementemia in 1/3 of patients and is beginning to be considered as a possible mechanism of platelet destruction [9]. Hypocomplementemia is observed in patients with severe thrombocytopenia, and the rate of progression from pITP to SLE is higher in such cases [10]. Thrombocytopenia is a frequently observed complication of SLE and was reported in 16.8% of 2104 SLE cases reviewed in China [11]. In that study, hypocomplementemia was identified in a multifactorial analysis as a factor correlated with thrombocytopenia, along with lupus nephritis and various other factors, but no specific decrease in complement protein or complement system abnormalities were mentioned [11].
Serum immune biomarker levels combined with hepatitis B virus infection status predict early recurrence of early-stage hepatocellular carcinoma with microvascular invasion after liver resection
Published in Acta Chirurgica Belgica, 2023
Xiaobo Wang, Yuanquan Zhao, Tao Bai, Jiazhou Ye, Shaolong Lu, Feixiang Wu, Lequn Li, Jie Chen
Humoral immunity also plays an indispensable role in the antitumor immune system, mainly by recognizing specific antigens on tumor cells through plasma cells; secreting various antibodies; and activating complement and cell-killing mechanisms, leading to tumor cell dissolution. Complement is an immune active substance in the body, predominantly composed of C3 and C4. Its function is to induce immune activity in the process of activation. Most of the complement C4 is produced in the liver and macrophages and injury of liver cells can lead to reductions in the serum complement level. Therefore, when lymphocytes infiltrate hepatoma, the secretory functions of hepatocytes and macrophages are inhibited, resulting in a decrease in complement C4, which ultimately weakens the inhibitory effect of complement on hepatoma [20,21].
Quantitative proteome profiling provides evidence of an activation of the complement cascade in ATTR amyloidosis
Published in Amyloid, 2021
Christian Treitz, Juliane Gottwald, Eva Gericke, Peter Urban, Rolf Rüdiger Meliß, Hans-Detlef Axmann, Frank Siebert, Karsten Becker, Andreas Tholey, Christoph Röcken
Apart from the fibril-forming protein, amyloid deposits often enclose various other non-amyloidogenic but seemingly disease-specific constituents, such as serum amyloid P-component (SAMP), apolipoprotein E (APOE), highly sulphated glycosaminoglycans, laminin, vitronectin (VTNC), apolipoprotein J (CLUS), among others [4–6]. These non-fibrillar constituents may not be simple passive bystanders of the disease. Instead, some have shown to be active contributors to disease initiation, progression, and possibly clearance [7–9]. In addition, proteomic analyses of amyloid occasionally report on the presence of members of the complement system [5,6,10]. The complement system is one of the principal immunologically relevant effector systems that comprises over 14 soluble proteins, a number of receptors and several soluble membrane proteins performing regulatory functions. Its major target are cell membranes. A direct attack that requires participation of all nine complement components leads to irreversible damage and subsequently ultrastructural lesions [11,12]. The terminal pathway is the assembly of the complement components (CO) CO5b, CO6, CO7, CO8, and multiple copies of CO9 into the membrane attack complex (MAC). MAC functions as a transmembrane channel [13–15], causing loss of membrane integrity leading to cell death by necrosis [16].
Related Knowledge Centers
- Adaptive Immune System
- Antibody
- Inflammation
- Innate Immune System
- Protein
- Immune System
- Liver
- Cell Membrane
- Phagocytosis
- Protein Precursor