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Order Picornavirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
Khor et al. (2002) created an antiviral against measles virus (MV) by displaying a peptide known to inhibit MV infection. This peptide sequence corresponded to a portion of the MV binding site on the human MV receptor CD46. The CPMV-CD46 chimera efficiently inhibited MV infection of HeLa cells in vitro, while wild-type CPMV did not. Furthermore, the CPMV-CD46 chimera protected mice from mortality induced by an intracranial challenge with MV. The CD46 peptide presented in the context of CPMV was up to 100-fold more effective than the soluble CD46 peptide at inhibiting MV infection in vitro (Khor et al. 2002). In fact, this study represented the first utilization of a plant virus chimera as an antiviral agent.
Measles and its neurological complications
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Benedikt Weissbrich, Jürgen Schneider-Schaulies
One of the most important characteristics determining viral tropism is the usage of specific receptors on the surface of susceptible target cells that allow viral attachment and penetration. MV is highly species specific in that it does not naturally replicate in nonprimate hosts. In vivo it reveals a pronounced tropism for cells of the hematopoietic lineage and epithelial cells. Multinucleated giant cells are formed in lymph nodes. They are pathognomonic for the measles infection. However, endothelial cells and neural cells such as neurons, astrocytes and microglial cells can also be infected. As cellular receptors for MV, the widely expressed transmembrane protein CD46 [12,13], the lymphoid cell specific signaling lymphocytic activation molecule (SLAM, CD150) [14,15], and the epithelial cell-specific receptor nectin-4 [16,17] have been identified. In contrast to CD46, which is utilized by vaccine and lab-adapted MV strains, all wild-type strains and isolates interact with CD150 on the surface of activated B and T cells, dendritic and memory cells, and with nectin-4 on epithelial cells.
Immune Control of Pregnancy
Published in Robert E. Garfield, Thomas N. Tabb, Control of Uterine Contractility, 2019
Gérard Chaouat, Elisabeth Menu, Valentine Djian, Genevieve Delage, Due Can Dang, Aines Assai Meliani, Jacques Martal, Sylvie Ropert
Concerning antibody plus complement, the placenta resists antibody plus complement mediated lysis, because it expresses at its surface the CD46 molecule, an integral member of the MCP (membrane cofactor for complement protein) DAF (decay accelerating factor) system16,92–94 and the other complement regulatory protein CD56. These functionally inactivate the complement activation pathway that is required to assure cell lysis once antibody is fixed at the membrane surface. Therefore, even cytotoxic antibodies become harmless and could act locally as blocking/enhancing ones. Incidentally, CD46 was found as a spinoff of the search for the so-called TLX antigens.95
Daratumumab induces cell-mediated cytotoxicity of primary effusion lymphoma and is active against refractory disease
Published in OncoImmunology, 2023
Prabha Shrestha, Yana Astter, David A. Davis, Ting Zhou, Constance M. Yuan, Ramya Ramaswami, Hao-Wei Wang, Kathryn Lurain, Robert Yarchoan
PEL generally expresses high levels of CD38, suggesting Dara may be a promising treatment option. Consistent with a recently published report by Panaampon et al.,43 we found that Dara can induce ADCC-mediated lysis of PEL cell lines, particularly those with high surface CD38 levels. However, in contrast to that study, we failed to find that Dara could induce CDC in the PEL cell lines tested. This difference may be attributed to our use of human serum as a source of complement as opposed to the rabbit serum used by Panaampon et al.43 Complement-inhibitory membrane proteins CD46, CD55, and CD59 are species-specific, inhibiting human but not non-human complement.44,45 All PEL cell lines expressed high levels of these proteins compared to Daudi, a BL cell line that readily shows Dara-induced CDC in the presence of human complements. Neutralizing both CD55 and CD59 on the PEL cell surface led to a significant albeit incomplete rescue of Dara-induced CDC of PEL cell lines, suggesting that expression of these proteins contributes to the resistance of PEL to Dara-mediated CDC. Additionally, inhibiting CD46 may further enhance Dara-induced CDC,46 although we were unable to test this directly.
Differentiation and Maturation Effect of All-Trans Retinoic Acid on Cultured Fetal RPE and Stem Cell-Derived RPE Cells for Cell-Based Therapy
Published in Current Eye Research, 2022
Tingyu Yan, Na Yang, Wei Hu, Xinxin Zhang, Xuedong Li, Youjin Wang, Jun Kong
Morphological changes and pigmentation do not represent all RPE functionalities. RPE plays complex roles, especially a major role in controlling the ocular immune response through the expression of various CRPs during the pathological process of AMD and Stargardts disease. Photoreceptors are critically dependent on a healthy RPE for continued viability.42 CRPs, such as CD46, CD55, and CD59, protect host cells from complement attack. CRPs in RPE cells are upregulated by inflammatory cytokines and repetitive nonlethal oxidant exposure in a species-specific manner. Increased CRPs expression may help to protect RPE cells from complement- and oxidant-mediated injury in AMD.43 Our results showed that stem cell-derived RPE cells have compromised CRPs expression compared with fRPE cells. It may be as important to obtain well-differentiated stem cells derived RPE cells with comparable CRPs expression as RPE markers for cell-based therapy.
Hyalocyte functions and immunology
Published in Expert Review of Ophthalmology, 2022
Stefaniya K Boneva, Julian Wolf, Peter Wieghofer, J Sebag, Clemens AK Lange
In addition to these indirect immunosupressive effects, hyalocytes are thought to reduce intraocular inflammation by contributing directly to an immunosuppressive milieu in the vitreous body in order to maintain vitreous transparency and visual function. Recent evidence suggests that hyalocytes express a variety of factors known to be key players in immune privilege of the eye, for instance, alpha-melanocyte-stimulating hormone (α-MSH), cluster of differentiation 86 (CD86), cluster of differentiation 46 (CD46), and TGF-β2 (Table 1). It is known from animal studies that TGF-β2 [71,72] and α-MSH [73] participate in the immune privilege by suppressing inflammatory responses of T helper cells [72] and inducing regulatory T cells [74]. Furthermore, in vitro studies have demonstrated that CD86-expressing iris pigmented epithelial cells are capable of preventing cell proliferation and cytokine secretion of T cells [75]. CD46, which functions as a regulator of the alternative complement pathway, is responsible for the suppression of adaptive T helper cells immune responses, thus protecting tissues from the autologous complement system [76]. The abundant expression of CD46 by hyalocytes (Table 1) and its presence in the human vitreous, may be yet another factor contributing to the immune-privileged microenvironment. Further research is warranted to elucidate the exact mechanisms underlying the immunosuppressive properties of hyalocytes in health, and potential pro-inflammatory properties in disease.