Immuno

6 pages, 210 KiB

Open AccessCase Report

Fulminant Recurrent Thrombosis in a Patient with Catastrophic Antiphospholipid Syndrome and Its Thirty-Day Outcome

by Pierpaolo Di Micco, Maurizio Dorato, Maurizio Latte, Maria D’Antò, Vittorio Luiso and Gerolamo Sibilio

Immuno 2024, 4(1), 125-130; https://doi.org/10.3390/immuno4010008 - 4 Mar 2024

Viewed by 1359

Abstract

Catastrophic antiphospholipid syndrome (CAPS) is a rare clinical form of antiphospholipid syndrome (APS) associated with life-threatening complications due to simultaneous thrombosis that may affect small and large vessels. It may be localized to the venous and/or arteries at the same time, and there [...] Read more.

Catastrophic antiphospholipid syndrome (CAPS) is a rare clinical form of antiphospholipid syndrome (APS) associated with life-threatening complications due to simultaneous thrombosis that may affect small and large vessels. It may be localized to the venous and/or arteries at the same time, and there are not available guidelines based on randomized clinical trials or large series. We here report a clinical case of CAPS with onset after resolution of oligo-symptomatic infection SARS-CoV-2, that had transient improvement with warfarin after recurrent thromboses occurred despite treatment off-label with low doses of low molecular weight heparin. Furthermore, we tried to trace a line by which a multidisciplinary team may set specific timing to have follow-up because of the high morbidity, mortality, and prolonged time of hospitalization. Full article

17 pages, 2911 KiB

Open AccessArticle

A Serological Multiplexed Immunoassay (MIA) Detects Antibody Reactivity to SARS-CoV-2 and Other Viral Pathogens in Liberia and Is Configurable as a Multiplexed Inhibition Test (MINT)

by Brien K. Haun, Albert To, Caitlin A. Williams, Aquena Ball, Karalyn Fong, Teri Ann S. Wong, Bode Shobayo, Julius Teahton, Lauren Ching, Varney Kamara, Davidetta M. Tekah, Peter Humphrey, John Berestecky, Vivek R. Nerurkar and Axel T. Lehrer

Immuno 2024, 4(1), 108-124; https://doi.org/10.3390/immuno4010007 - 3 Mar 2024

Viewed by 2321

Abstract

The SARS-CoV-2 pandemic ignited global efforts to rapidly develop testing, therapeutics, and vaccines. However, the rewards of these efforts were slow to reach many low- to middle-income countries (LMIC) across the African continent and globally. Therefore, two bead-based multiplexed serological assays were developed [...] Read more.

The SARS-CoV-2 pandemic ignited global efforts to rapidly develop testing, therapeutics, and vaccines. However, the rewards of these efforts were slow to reach many low- to middle-income countries (LMIC) across the African continent and globally. Therefore, two bead-based multiplexed serological assays were developed to determine SARS-CoV-2 exposure across four counties in Liberia. This study was conducted during the summer of 2021 on 189 samples collected throughout Grand Bassa, Bong, Margibi, and Montserrado counties. Our multiplexed immunoassay (MIA) detected elevated exposure to SARS-CoV-2 and multiple variant antigens. Additionally, we detected evidence of exposure to Dengue virus serotype 2, Chikungunya virus, and the seasonal coronavirus NL63. Our multiplexed inhibition test (MINT) was developed from the MIA to observe antibody-mediated inhibition of SARS-CoV-2 spike protein binding to its cognate cellular receptor ACE-2. We detected inhibitory antibodies in the tested Liberian samples, which were collectively consistent with a convalescent serological profile. These complementary assays serve to supplement existing serological testing needs and may enhance the technical capacity of scientifically underrepresented regions globally. Full article

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17 pages, 2047 KiB

Open AccessReview

Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 Diabetes

by Dequina A. Nicholas, Jacques C. Mbongue, Darysbel Garcia-Pérez, Dane Sorensen, Heather Ferguson Bennit, Marino De Leon and William H. R. Langridge

Immuno 2024, 4(1), 91-107; https://doi.org/10.3390/immuno4010006 - 1 Mar 2024

Cited by 3 | Viewed by 2748

Abstract

Around 285 million people worldwide currently have type 2 diabetes and it is projected that this number will be surpassed by 2030. Therefore, it is of the utmost importance to enhance our comprehension of the disease’s development. The regulation of diet, obesity, and [...] Read more.

Around 285 million people worldwide currently have type 2 diabetes and it is projected that this number will be surpassed by 2030. Therefore, it is of the utmost importance to enhance our comprehension of the disease’s development. The regulation of diet, obesity, and inflammation in type 2 diabetes is believed to play a crucial role in enhancing insulin sensitivity and reducing the risk of onset diabetes. Obesity leads to an increase in visceral adipose tissue, which is a prominent site of inflammation in type 2 diabetes. Dyslipidemia, on the other hand, plays a significant role in attracting activated immune cells such as macrophages, dendritic cells, T cells, NK cells, and B cells to visceral adipose tissue. These immune cells are a primary source of pro-inflammatory cytokines that are believed to promote insulin resistance. This review delves into the influence of elevated dietary free saturated fatty acids and examines the cellular and molecular factors associated with insulin resistance in the initiation of inflammation induced by obesity. Furthermore, it explores novel concepts related to diet-induced inflammation and its relationship with type 2 diabetes. Full article

(This article belongs to the Section Innate Immunity and Inflammation)

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14 pages, 4373 KiB

Open AccessArticle

IL-12p40 Monomer: A Potential Player in Macrophage Regulation

by Brian Jeong and Kalipada Pahan

Immuno 2024, 4(1), 77-90; https://doi.org/10.3390/immuno4010005 - 23 Feb 2024

Cited by 1 | Viewed by 1835

Abstract

Macrophages are myeloid phagocytic leukocytes whose functions are to protect against infections, mediate T-cell responses, and maintain tissue homeostasis. IL-12p40 monomer is a cytokine that is largely produced by macrophages, and it has, for the longest time, been considered a largely non-functional cytokine [...] Read more.

Macrophages are myeloid phagocytic leukocytes whose functions are to protect against infections, mediate T-cell responses, and maintain tissue homeostasis. IL-12p40 monomer is a cytokine that is largely produced by macrophages, and it has, for the longest time, been considered a largely non-functional cytokine of the IL-12 family. However, new research has emerged that demonstrates that this p40 monomer may play a bigger role in shaping immune environments. To shed light on the specific effects of p40 monomer on macrophages and their surrounding environment, we showed, through cell culture studies, qPCR, ELISA, and immunofluorescence analyses, that the direct administration of recombinant p40 monomer to RAW 264.7 cells and primary lung macrophages stimulated the production of both pro-inflammatory (TNFα) and anti-inflammatory (IL-10) signals. Accordingly, p40 monomer prevented the full pro-inflammatory effects of LPS, and the neutralization of p40 monomer by mAb a3-3a stimulated the pro-inflammatory effects of LPS. Furthermore, we demonstrated that the intranasal administration of p40 monomer upregulated TNFα⁺IL-10⁺ macrophages in vivo in the lungs of mice. Collectively, these results indicate an important immunoregulatory function of p40 monomer in the upregulation of both pro- and anti-inflammatory molecules in macrophages. Full article

(This article belongs to the Section Autoimmunity and Immunoregulation)

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20 pages, 716 KiB

Open AccessReview

Immune Dysregulation and Current Targeted Biologics in Hidradenitis Suppurativa

by Rene Chen, Robyn Guo, Amy J. Petty and Tarannum Jaleel

Immuno 2024, 4(1), 57-76; https://doi.org/10.3390/immuno4010004 - 2 Feb 2024

Viewed by 2603

Abstract

Hidradenitis Suppurativa (HS) is a debilitating cutaneous disease characterized by a vicious cycle of chronic inflammation and tissue destruction that stems from disruption of the skin microbiome and abnormal activation of both the innate and adaptive immune system. A hallmark of HS pathophysiology [...] Read more.

Hidradenitis Suppurativa (HS) is a debilitating cutaneous disease characterized by a vicious cycle of chronic inflammation and tissue destruction that stems from disruption of the skin microbiome and abnormal activation of both the innate and adaptive immune system. A hallmark of HS pathophysiology is dysregulation of both the innate and adaptive immune system. The role of immune system dysregulation in HS development has motivated researchers to explore the utility of biologic immunomodulators. In 2015, adalimumab, a tumor necrosis factor-α inhibitor, was approved by the Food and Drug Administration (FDA) for treatment of moderate-to-severe HS in the US. In 2023, secukinumab, an interleukin-17A (IL-17A) inhibitor, was approved by the European Medicines Agency for treatment of moderate-to-severe HS in Europe. Ongoing clinical trials have shown promising clinical responses to targeted therapies against other pro-inflammatory cytokines including IL-17, IL-12, IL-1, IL-36, IL-6, IL-10, interferon γ, C5a, and Janus kinase (JAK). We provide an update on the efficacy and clinical usage of targeted biologics in HS treatment. Full article

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14 pages, 2070 KiB

Open AccessArticle

Markers for Immunological Resilience: Effects of Moderate- and High-Intensity Endurance Exercise on the Kinetic Response of Leukocyte Subsets

by Shirley W. Kartaram, Marc Teunis, Klaske van Norren, Mieke Smits, Laura M’Rabet, Martie C. M. Verschuren, Karin Mohrmann, Johan Garssen, Renger Witkamp and Raymond Pieters

Immuno 2024, 4(1), 43-56; https://doi.org/10.3390/immuno4010003 - 30 Jan 2024

Viewed by 1862

Abstract

The kinetic responses of leukocyte subsets to exercise and their recovery may serve as indicators of immunological resilience. These time-dependent responses were investigated in healthy young men using a bicycle ergometer test. Fifteen recreationally active male cyclists (20–35 years, VO_2max 56.9 ± [...] Read more.

The kinetic responses of leukocyte subsets to exercise and their recovery may serve as indicators of immunological resilience. These time-dependent responses were investigated in healthy young men using a bicycle ergometer test. Fifteen recreationally active male cyclists (20–35 years, VO_2max 56.9 ± 3.9 mL kg⁻¹ min⁻¹) performed four exercise protocols with a 1 h duration in a cross-over design: at 70% of the maximal workload (Wmax) in a hydrated and a mildly dehydrated state, at 50% of the Wmax, and intermittently at 85/55% of the Wmax in blocks of 2 min. The numbers of lymphocytes, monocytes, neutrophils, eosinophils, basophils, thrombocytes, and NK cells (CD16 and CD56) were measured at different time points up to 24 h post-exercise. The total leukocyte counts and those of most subsets increased from the start of the exercise, peaking after 30–60 min of exercising. The neutrophil numbers, however, peaked 3 h post-exercise. The CD16^brightCD56^dim NK cells showed a 1.5-fold increase compared to the CD16^brightCD56^bright NK cells. Other than for MCP-1, no significant differences were found in the serum cytokine levels. Our results show that exercise intensity is reflected in different time-dependent changes in leukocyte subsets, which supports the concept that the exchange of immune cells between peripheral blood and tissues contributes to enhanced immune surveillance during strenuous exercise. Full article

(This article belongs to the Section Clinical/translational Immunology)

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29 pages, 3321 KiB

Open AccessReview

The Role of Structural Bioinformatics in Understanding Tumor Necrosis Factor α-Interacting Protein Mechanisms in Chronic Inflammatory Diseases: A Review

by Luana Luiza Bastos, Diego Mariano, Rafael Pereira Lemos, Tatiane Senna Bialves, Carlo Jose Freire Oliveira and Raquel C. de Melo-Minardi

Immuno 2024, 4(1), 14-42; https://doi.org/10.3390/immuno4010002 - 15 Jan 2024

Viewed by 3287

Abstract

Tumor necrosis factor α (TNF-α) is a multifunctional cytokine protein acknowledged as a vital mediator in cell differentiation, proliferation, and survival. Additionally, TNF-α is a crucial component of the host’s defense by mediating inflammatory and immune responses against various aggressive agents, including viruses, [...] Read more.

Tumor necrosis factor α (TNF-α) is a multifunctional cytokine protein acknowledged as a vital mediator in cell differentiation, proliferation, and survival. Additionally, TNF-α is a crucial component of the host’s defense by mediating inflammatory and immune responses against various aggressive agents, including viruses, bacteria parasites, and tumors. However, excessive production can be detrimental to the body and is also implicated in developing several inflammatory and immune-mediated disorders. Therefore, there is great interest in studying its role and its modulation, in various diseases, both in in vitro, in vivo, and in silico experiments. In this review, we evaluated the structures of proteins related to TNF-α available in public databases. In addition, we described the main antibodies blocking this cytokine and its applications and commented on the potential of naturally produced binding molecules, such as TNF-α-binding proteins produced by ticks. We also discuss the role of structural bioinformatics techniques in understanding the mechanisms of chronic inflammatory diseases related to TNF-α. We hope that the data presented in this review will be useful for studies that aim to better understand the mechanisms of the interactions of TNF-α with other proteins and will lead to new drugs or treatments. Full article

(This article belongs to the Section Structural Immunology)

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13 pages, 968 KiB

Open AccessReview

Catastrophic Antiphospholipid Syndrome: A Review

by Carmine Siniscalchi, Manuela Basaglia, Michele Riva, Michele Meschi, Tiziana Meschi, Giampiero Castaldo and Pierpaolo Di Micco

Immuno 2024, 4(1), 1-13; https://doi.org/10.3390/immuno4010001 - 25 Dec 2023

Cited by 6 | Viewed by 8292

Abstract

Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thrombotic or obstetric events occurring in individuals who have persistent antiphospholipid antibodies. Catastrophic antiphospholipid syndrome (CAPS) is a rare and potentially fatal form of APS characterized by severe thrombotic complications occurring in multiple [...] Read more.

Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thrombotic or obstetric events occurring in individuals who have persistent antiphospholipid antibodies. Catastrophic antiphospholipid syndrome (CAPS) is a rare and potentially fatal form of APS characterized by severe thrombotic complications occurring in multiple organs over a short period of time or simultaneously. CAPS is associated with a high (50%) death rate. Infections, multi-organ failure, and cerebral and heart thrombosis represent the main complications of this syndrome. Generally, anticoagulants, glucocorticoids, therapeutic plasmapheresis (TPE), and intravenous immunoglobulin (IVIG) are used in combination for treatment. Multidisciplinary care involving different specialists from hematology, rheumatology, nephrology, infectious disease, critical care, and obstetrics is often required due to the complexity of the disease. Recent data emphasize the effectiveness of biologics such as anti-TNF-a monoclonal antibodies (adalimumab, certolizumab), anti-CD38 monoclonal antibody (daratumumab), BAFF/Blys inhibitor (belimumab), and BTK inhibitor (zanubrutinib) against CAPS. In order to understand the underlying causes of CAPS, one future possibility involves investigating and characterizing the hereditary and acquired risk factors associated with CAPS. Full article

(This article belongs to the Special Issue Recent Advances in Antiphospholipid Syndrome)

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Immuno, Volume 4, Issue 1 (March 2024) – 8 articles

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