Immunology Case Reports

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Opinion Article - Immunology Case Reports (2023) Volume 6, Issue 2

Humoral innate immune component interactions with bacteria and viruses.

Lindsa Nichols*

Department of Microbiology, University of Bristol, United Kingdom

*Corresponding Author:
Lindsa Nichols
Department of Microbiology
University of Bristol, United Kingdom
E-mail:lnicholson@bristol.ac.uk

Received:30-Mar-2023, Manuscript No. AAICR-23-90266; Editor assigned:03-Apr-2023, PreQC No. AAICR-23-90266(PQ); Reviewed:17-Apr-2023, QC No. AAICR-23-90266; Revised:21-Apr-2023, Manuscript No. AAICR-23-90266(R); Published:28-Apr-2023, DOI:10.35841/aaicr-6.2.138

Citation: Nichols L. Humoral innate immune component interactions with bacteria and viruses. Immunol Case Rep. 2023;6(2):138

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Introduction

There are cellular and humoral components to the innate immune response. The cellular component includes many cell types that identify and eliminate infections and cellular waste using pattern recognition molecules. In the past two decades, a great deal of research has been paid to the interactions of pattern recognition molecules within the cellular component. About the interactions between the humoral elements, however, less is understood. The serine protease cascades of the complement and contact systems, as well as naturally occurring antibodies (NAb) and pentraxins, make up the humoral innate immune response[1].

In order to effectively defend the host against bacterial infections, several humoral innate immune system components must work together in a coordinated attack. A weak humoral innate immune system makes people more vulnerable to germs. Understanding how the complement and contact cascades, as well as NAb and pentraxins, interact is necessary for the development of treatments that reduce bacterial infections [2].

In addition to indirectly activating other immune system elements that fight bacteria, complement directly contributes to the humoral innate immune response by causing holes to develop in the bacteria's membrane and lysing them. The three start mechanisms for complement activation are activated by invading microorganisms. NAb detect bacterial invasion and initiate the mannose binding lectin complement cascade. Furthermore, sugar moieties on bacterial surfaces are recognised by the mannose binding lectin pathway. Moreover, the alternative complement pathway is triggered by the presence of bacterial proteins, lipids, and carbohydrates. C3 cleaves into C3b when all three routes are activated. C3b covers the bacterial surface and, through the process of opsonization, improves neutrophil and macrophage recognition. Furthermore, C3b coated bacteria bind CR2 to increase Ab synthesis. Bacterial lysis by membrane attack complex may also result from any of the aforementioned mechanisms of initiation [3].

Many NAb can identify commensals, such as Salmonella typhosa and enterics like E. coli. The presence of NAb prevents the gut microbiota and enterics from overgrowing. The respiratory pathogen S. pneumonia is also protected by NAb. Pneumococcal antigens may induce the creation of these Ab since they first colonise newborns' respiratory tracts. NAb not only control commensals but are also essential for preventing the spread of intracellular bacteria. For instance, NAb promote Listeria monocytogenes antigen-trapping in secondary lymphoid organs.

With Viruses

Complement functions as a mediator between the innate and adaptive immune systems, a component of humoral immunity, and can directly kill viruses and control pathogen eradication. The HIV, SARS coronavirus, and Marburg virus are just a few of the viral glycoproteins that the mannose binding lectin directly binds. Moreover, CR1 is bound by C3-coated glycoproteins, which improves the humoral immune response. Similar to this, iC3b, C3dg, and C3d are recognised by CR2 to lower the B cell activation threshold. Moreover, complement activation plays a critical role in the immune response to viruses as shown by the contribution of C1q, C3, C4, and CR1 and CR2 to the regular antiviral IgM or IgG responses and modulation of humoral immunity [4].

By encoding viral proteins with structural and functional similarities to host proteins or by luring host complement regulatory proteins to the virion, viruses can also influence the regulators of complement activation. A complement inhibitory protein, for instance, is expressed on the cell surface as a result of the gamma-herpes virus 68 infection and can be found in the supernatants of infected cells. The viral inhibitory proteins prevent C3 deposition by both the traditional and alternative activation pathways, according to in vitro investigations. The complement cascade regulators that bind C3b or C4b and inhibit activity are also encoded by the Kaposi's sarcoma-associated herpes virus, Herpes saimiri, Variola, Vaccinia, Monkeypox, and Ectromelia viruses. To avoid being destroyed by complement, other viruses add host complement regulating proteins to their virions. To evade the complement response, human cytomegalovirus, human T-lymphotropic virus, and human immunodeficiency virus-1 all integrate the complement control proteins CD55 and CD59 into their virions. Complement inhibitors, whether produced by the host or by the virus, prevent the infected cell from lysing and promote virus growth [5].

Conclusion

The inflammatory response is started and controlled by the humoral immune system, which also helps to get rid of germs. Components of the innate humoral immune response, which are derived from several tiny plasma proteins, damage the target cell's plasma membrane and cause cytolysis. The humoral and cellular immune responses work in tandem to stop the multiplication of bacteria and viruses as well as infected and abnormal cells. Pathogens have developed ways to thwart and elude the immune response, though. Moreover, unchecked cancer cells and atherosclerotic lesions may take advantage of the humoral innate response to continue growing despite the humoral immune response.

References

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