A5084693520- Complement system in diseases
- Influenza Virus Research Studies
- Neonatal Respiratory Health Research
- SARS-CoV-2 and COVID-19 Research
- Immune Response and Inflammation
- Respiratory viral infections research
- Platelet Disorders and Treatments
- COVID-19 Clinical Research Studies
- Viral Infections and Outbreaks Research
- Immune cells in cancer
- HIV Research and Treatment
- Mycobacterium research and diagnosis
- Virology and Viral Diseases
- Extracellular vesicles in disease
- Mosquito-borne diseases and control
- Blood groups and transfusion
- Fibroblast Growth Factor Research
- Blood properties and coagulation
- COVID-19 Impact on Reproduction
- Blood Coagulation and Thrombosis Mechanisms
- Tuberculosis Research and Epidemiology
- Galectins and Cancer Biology
- Leprosy Research and Treatment
- Infectious Diseases and Tuberculosis
- Proteoglycans and glycosaminoglycans research
Brunel University of London
2018-2024
Vellore Institute of Technology University
2020-2024
Coronavirus disease (COVID-19) is an acute infectious caused by the severe respiratory syndrome coronavirus 2 (SARS-CoV-2). Human SP-D (surfactant protein D) known to interact with spike of SARS-CoV, but its immune surveillance against SARS-CoV-2 not known. The current study aimed examine potential a recombinant fragment human (rfhSP-D) as inhibitor replication and infection SARS-CoV-2. interaction rfhSP-D ACE-2 (angiotensin-converting enzyme 2) receptor was predicted via docking analysis....
C4b Binding Protein (C4BP) is a major fluid phase inhibitor of the classical and lectin pathways complement system. Complement inhibition achieved by binding to restricting role activated component C4b. C4BP functions as co-factor for factor I in proteolytic inactivation both soluble cell surface-bound C4b, thus formation C3-convertase, C4b2a. also accelerates natural decay/dissociation C3 convertase. This makes prime target exploitation pathogens escape attack, seen Streptococcus pyogenes...
Surfactant protein D (SP-D), a C-type collagen containing lectin (collectin), is expressed in the mucosal secretion of lung and contribute to innate host defence against variety pathogens, including influenza A virus (IAV). SP-D has been shown inhibit haemagglutination activity infectivity IAV, addition reducing neuraminidase (NA) activity. exhibits strong anti-IAV by virtue its carbohydrate recognition domain (CRD) binding pattern (N-linked mannosylated) on NA hemagglutinin (HA) IAV. Here,...
Human Surfactant Protein (SP-D) is a potent innate immune molecule, which emerging as key molecule in the recognition and clearance of altered non-self targets. Previous studies have shown that recombinant fragment human SP-D (rfhSP-D) induced apoptosis via p53 mediated pathway an eosinophilic leukemic cell line, AML14.3D10. Here, we report ability rfhSP-D to induce TNF-α/Fas-mediated regardless status pancreatic adenocarcinoma using Panc-1 (p53mt), MiaPaCa-2 Capan-2 (p53wt) lines. Treatment...
The Influenza A virus (IAV) is a severe respiratory pathogen. C1q the first subcomponent of complement system's classical pathway. composed 18 polypeptide chains. Each these chains contains collagen-like region located at N terminus, and C-terminal globular head organized as heterotrimeric structure (ghA, ghB ghC). This study was aimed investigating activation-independent modulation by its individual recombinant heads against IAV infection. interaction with purified glycoproteins examined...
The complement system is a key component of the innate immune response to viruses and proinflammatory events. Exaggerated activation has been attributed induction cytokine storm in severe SARS-CoV-2 infection. However, there also an argument for protective role proteins, given their local synthesis or at site viral This study investigated activation-independent C1q C4b-binding protein (C4BP) against interactions C1q, its recombinant globular heads, C4BP with spike receptor binding domain...
The classical pathway of the complement system is activated by binding C1q in C1 complex to target activator, including immune complexes. Factor H regarded as key downregulatory protein alternative pathway. However, both and factor bind surfaces via charge distribution patterns. For a few targets, compete for common or overlapping sites. H, therefore, can effectively regulate activation through such addition its previously characterized role Both are known recognize foreign altered-self...
The complement system is readily triggered by the presence of damage-associated molecular patterns on surface tumor cells. alternative pathway provides rapid amplification stress signal, leading to cascade activation deal with pathogens or malignant Properdin only known positive regulator pathway. In addition, properdin promotes phagocytic uptake apoptotic T cells macrophages and dendritic without activating system, thus, establishing its ability recognize “altered-self”. Dysregulation has...
Human surfactant protein D (SP-D) belongs to the family of collectins that is composed a characteristic amino-terminal collagenous region and carboxy-terminal C-type lectin domain. Being present at mucosal surfaces, SP-D acts as potent innate immune molecule offers protection against non-self altered self-such pathogens, allergens, tumour. Here, we examined effect recombinant fragment human (rfhSP-D) on range breast cancer lines. Breast has four molecular subtypes characterised by varied...
The complement system is designed to recognise and eliminate invading pathogens via activation of classical, alternative lectin pathways. Human properdin stabilises the pathway C3 convertase, resulting in an amplification loop that leads formation C5 thereby acting as a positive regulator pathway. It has been noted human on its own can operate pattern recognition receptor exert immune functions outside involvement activation. Properdin bind directly microbial targets DNA, sulfatides...
The complement system is an ancient innate immune defence mechanism that can recognise molecular patterns on the invading pathogens. Factor H, as inhibitor of alternative pathway, down-regulates activation host cell surface. Locally synthesised factor H at site infection/injury, including lungs, act a pattern recognition molecule without involving activation. Here, we report sialic acid binder, interacts with influenza A virus (IAV) and modulates IAV replication, observed by upregulation...
Lung surfactant protein D (SP-D) and Dendritic cell-specific intercellular adhesion molecules-3 grabbing non-integrin (DC-SIGN) are pathogen recognising C-type lectin receptors. SP-D has a crucial immune function in detecting clearing pulmonary pathogens; DC-SIGN is involved facilitating dendritic cell interaction with naïve T cells to mount an anti-viral response. have been shown interact various viruses, including SARS-CoV-2, enveloped RNA virus that causes COVID-19. A recombinant fragment...
Abstract Rationale COVID-19 is an acute infectious disease caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Human surfactant protein D (SP-D) known to interact with spike of SARS-CoV, but its immune-surveillance against SARS-CoV-2 not known. Objective This study aimed examine potential a recombinant fragment human SP-D (rfhSP-D) as inhibitor replication and infection SARS-CoV-2. Methods rfhSP-D interaction hACE-2 receptor was predicted via docking analysis. The...
Abstract Factor B, a serine protease proenzyme and part of the complement system, binds to other proteins such as C3b properdin. While it is known be activated by factor D, interactions that interfere with binding between B are less well-understood. We attached thiol Sepharose via its free SH group conducted competition assay employing 125 I-labelled study competitive binding. Two anti-C3d monoclonal antibodies (F49b 4C2) were found partially inhibit C3b. The inhibitory effects these...
Abstract Severe cases of SARS-CoV-2 infection are characterised by an imbalanced immune response, excessive inflammation, and the development acute respiratory distress syndrome, which can lead to multiorgan failure death. Several studies have demonstrated dysregulated complement activity as indicator immunopathogenesis in infection. Notably, alternative pathway has been implicated driving inflammation during severe Reduced levels factor H (FH), a down-regulator pathway, increased properdin...
Abstract The classical pathway of the complement system is activated by binding C1q in C1 complex to target activator including immune complexes. Factor H regarded as key downregulatory protein alternative complement. However, and factor both bind surfaces via charge distribution patterns. For few targets, compete for common or overlapping sites. H, therefore, can effectively regulate activation such addition its previously characterized role pathway. Both are reported recognize “foreign”...
ABSTRACT Due to profound heterogeneity within stromal immune tumor microenvironment (TME), pancreatic ductal adenocarcinoma (PDAC) remains a hard treat disease, with the lowest 5-year survival below 10%. Large-scale transcriptomic analysis has revealed two main, clinically relevant PDAC signatures: therapy responsive ‘Classical’ subtype better prognosis, and poorly-differentiated Basal-like poor prognosis. It also become evident that cellular humoral components in TME considerably influence...
Abstract Pattern recognition receptors are crucial for innate anti-viral immunity, including C-type lectin receptors. Two such examples Lung surfactant protein D (SP-D) and Dendritic cell-specific intercellular adhesion molecules-3 grabbing non-integrin (DC-SIGN) which soluble membrane-bound receptors, respectively. SP-D has a immune function in detecting clearing pulmonary pathogens; DC-SIGN is involved facilitating dendritic cell interaction as an antigen-presenting with naïve T cells to...