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Complement-Mediated Lipopolysaccharide Release
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Some facultative intracellular pathogens not only evade complement-mediated killing but have also evolved the capacity to utilize complement receptors to gain entry into host cells. The intracellular fate of some opsonized intracellular bacterial pathogens, such as salmonellae, may be dependent on the complement receptor engaged by the organism. CR1 (CD35)-mediated binding and internalization of Salmonella is associated with intracellular survival, while CR3 (CD11b/CD 18)-mediated binding leads to bacteriolysis (75). The mechanism for the differential fates of CR1-bound versus CR3-bound bacteria is not known. However, earlier studies suggested that bacteria-phagocyte receptor interactions influence the granule constituents ultimately found in the neutrophil phagosome. When S. typhimurium were coated with IgG or C3b, radioiodinated azurophilic granule proteins were abundant in the phagosome, as were labeled FcR and C3b receptor molecules. In contrast, phagosomes containing Salmonella internalized by IgG-FcR interactions contained specific granule proteins, while bacteria opsonized with C3b failed to trigger the release of specific granule proteins into the phagosome (76).
Inflammation and Cytokines in Airway Wall Remodelling
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
A number of differences have been described between normal and asthmatic peripheral blood monocytes. Monocytes from asthmatic subjects bear more FcεRII receptors, which may be suppressed by corticosteroids.265,281 They also show enhanced complement receptor expression.282
Host Defense I: Non-specific Immunity
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
First identified were the receptors for C3b and its fragments. These have been designated CR(“complement receptor”) 1–5. CR1 (also called CD35,) on erythrocytes, B and T cells, phagocytic cells, and dendritic cells, is a receptor for C3b and iC3b, and mediates their opsonic actions. CR2 (a.k.a. CD21) of
Autoimmune disorders associated with common variable immunodeficiency: prediction, diagnosis, and treatment
Published in Expert Review of Clinical Immunology, 2022
Niloufar Yazdanpanah, Nima Rezaei
Complement receptor type 2 (CR2, also known as CD21) is expressed on different immune cells. On B cells, CD21 contributes to the formation of a complex with CD19 and CD81. The complex acts as a coreceptor for the B cell receptor (BCR), which decreases the threshold of B cell activation upon stimulation [43,44]. B cells express CD21 based on their maturation stage; circulating naïve B cells and memory B cells express higher levels of CD21 compared to plasma cells [45]. A genetic defect of CD21 is associated with hypogammaglobulinemia [46]. Current data underpins that CD21low B cells derive from either memory B cells or plasma cells following chronic stimulation with extrinsic antigens [47]. CD21low B cells have shown weak proliferation through BCR signaling and demonstrated a shorter half-life compared with CD21+ B cells. Furthermore, despite representing an activated phenotype, CD21low B cells express inhibitory receptors. On the other hand, expansion of CD21low B cells was reported in autoreactive clones of immune cells [48–50]. Rakhmanov et al. described CD21low B cells as pre-activated polyclonal cells, which represent an attenuated function and are mainly localized in peripheral tissues [51]. Following provocation via CD40L, IL-2, and IL-10, CD21low B cells release higher levels of IgM in comparison with naïve B cells; high IgM level is proposed to be linked with the development of autoimmune conditions in CVID patients [14,52,53].
Innate Lymphoid Cells and Adaptive Immune Cells Cross-Talk: A Secret Talk Revealed in Immune Homeostasis and Different Inflammatory Conditions
Published in International Reviews of Immunology, 2021
The inflammatory immune response has evolved to protect the host from invading pathogens and the danger or damage-associated molecular patterns (DAMPs) originated within the host as a consequence of different physiological or pathophysiological processes. The innate immune cells through their pattern recognition receptors (PRRs) recognize microbe-associated molecular patterns (MAMPs)/pathogen-associated molecular patterns (PAMPs), and DAMPs, which controls several immune mechanisms (release of cytokines, chemokines, reactive oxygen and nitrogen species (ROS and RNS), and phagocytosis) involved in generating inflammatory immune response [1, 2]. For example, phagocytosis is one of the several mechanisms to contain the infection, MAMPs, and DAMPs [2]. However, phagocytosis also controls the generation of inflammatory immune response. For example, phagocytosis of the apoptotic cells is non-inflammatory but is pro-inflammatory in case of cell death due to necrosis, necroptosis, and ferroptosis [2, 3]. Phagocytosis clears apoptotic cells more efficiently than cells dying due to necroptosis and ferroptosis causing inflammation [4, 5]. The ferroptosis of macrophages during Mycobacterium tuberculosis infection in response to the phagocytosis of the pathogen causes their necrotic cell death causing pro-inflammatory lung damage associated with tuberculosis (TB) [6, 7]. Complement system (CS) also serves as a humoral component of innate immunity to control inflammation, although, both innate and adaptive immune cells along with different PRRs express complement receptors (CRs) [8].
Role of Mac-1 integrin in generation of extracellular vesicles with antibacterial capacity from neutrophilic granulocytes
Published in Journal of Extracellular Vesicles, 2020
Ákos M. Lőrincz, Balázs Bartos, Dávid Szombath, Viktória Szeifert, Csaba I. Timár, Lilla Turiák, László Drahos, Ágnes Kittel, Dániel S. Veres, Ferenc Kolonics, Attila Mócsai, Erzsébet Ligeti
To test the involvement of the two opsonin receptor types separately and independently from phagocytosis, we used relevant adhesive surfaces. Participation of Fc receptors in EV formation was investigated on immune complex surface but we did not observe significant increase of EV generation as compared to the control where Fc receptors are not activated (Figure 2(b)). In parallel experiments, we verified that neutrophils adherent to the immune complex surface were able to produce superoxide (Figure S3o), indicating that activation of the Fc receptors did take place and the lack of EV production increase was not the result of missing cell activation. Next we examined the potential role of complement receptors. On neutrophils the dominant complement receptors are CR3 and CR4, which belong to the family of β2 integrins and can be specifically activated by the complement fragment C3bi [44]. As shown in Figure 2(c), adding human PMN on a C3bi surface resulted in a significant increase in the number of detectable EVs. Thus, activation of the complement receptors is effective in EV biogenesis also in the absence of phagocytosis.