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In 2021, 273 Rocky Mountain Spotted Fever cases have been reported nationwide. In Chihuahua City, fourteen samples were obtained from children suspected of rickettsial infection. The analysis of samples collected from January to December 2021 showed a prevalence of 28.5%, 43% and 28.5% for Rickettsia rickettsii, Ehrlichia canis, and both pathogens in coinfection, respectively. The analysis of clinical hematological and biochemistry analytes showed alterations such as 100% of the children coursed with elevated liver enzymes and coagulation times, 64% showed leukocytosis due to neutrophilia, 55% of them had thrombocytopenia, lymphopenia and hypoalbuminemia, and 45% showed normocytic normochromic anemia. Statistically significant differences were obtained in the chemokines IL-8, RANTES, CXCL9/MIG, and CXCL10/IP-10 across the coinfected and control groups; the differences in IP-10 were significant for patients infected by R. rickettsii compared to the control group. Also, significant differences were observed for IL-1β, IL-6, IL-17, IFNγ, and TNFα among the R. rickettsii positive group compared to the control group; on the other hand; the coinfected group exhibited modified levels of IL-6, IL-8, and IL-10 compared with the control group. Finally, significant differences were obtained for CD8 + T lymphocytes subpopulations between positive individuals for R. rickettsii and E. canis.

Conventional rehabilitation strategies for stroke survivors become difficult when voluntary movements are severely disturbed. Combining passive limb mobilization, robotic devices and EEG-based brain-computer interfaces (BCI) systems might improve treatment and clinical follow-up of these patients, but detailed knowledge of neurophysiological mechanisms involved in functional recovery, which might help for tailoring stroke treatment strategies, is lacking. Movement-related EEG changes (EEG event-related desynchronization (ERD) in [Formula: see text] and [Formula: see text] bands, an indicator of motor cortex activation traditionally used for BCI systems), were evaluated in a group of 23 paralyzed chronic stroke patients in two unilateral motor tasks alternating paretic and healthy hands ((i) passive movement, using a hand exoskeleton, and (ii) voluntary movement), and compared to nine healthy subjects. In tasks using unaffected hand, we observed an increase of contralesional hemisphere activation for stroke patients group. Unexpectedly, when using paralyzed hand, motor cortex activation was reduced or absent in severely affected group of patients, while patients with moderate motor deficit showed an activation greater than control group. Cortical activation was reduced or absent in damaged hemisphere of all the patients in both tasks. Significant differences related to severity of motor deficit were found in the time course of [Formula: see text]-[Formula: see text] bands power ratio in EEG of contralesional hemisphere while moving affected hand. These findings suggest the presence of different compensation mechanisms in contralesional hemisphere of stroke patients related to the grade of motor disability, that might turn quantitative EEG during a movement task, obtained from a BCI system controlling a robotic device included in a rehabilitation task, into a valuable tool for monitoring clinical progression, evaluating recovery, and tailoring treatment of stroke patients.

Context: CD4+ T lymphocytes are able to differentiate into distinct subtypes according to several immunological scenarios, including T helper (Th)1, Th2, Th17 and regulatory T (Treg) cells. CD4+ T cells are phenotypically flexible and have specific ion channels, such as the nicotinic acetylcholine receptors (nAChR) that could be modulated by peptides produced by marine snails, known as conotoxins. Their effect on T lymphocytes has not been explored and emerging evidence suggests that these peptides may have immunomodulatory activities. Objective: This study investigated the effect of two Californiconus californicus-derived synthetic conotoxins on the proliferation and differentiation of T lymphocyte subpopulations Th1, Th2, Th17 and Treg. Methods: Cells from lymph nodes of BALB/c mice were cultured in the presence of conotoxins cal14.1b and cal14.2c (5.5 μM), during 96 h. Cell proliferation and intracellular cytokine production (IFN-γ, IL-4, IL-17 and IL-10) were analyzed by flow cytometry. Results and Discussion: cal14.1b and cal14.2c increased intracellular IL-10 production in Treg (CD3+CD4+Foxp3+) cells and decreased intracellular IL-17 production (CD3+CD4+) after 72 h of culture. Conotoxins did not show any effect on T cell proliferation nor Th1/Th2 balance. Conclusion: These results suggest that synthetic conotoxins exert immunomodulatory activity, especially by regulating specific functions on T lymphocytes.

As dendritic cells (DCs) are among the first cells to encounter antigens, these cells trigger both innate and T cell responses, and are the most potent antigen-presenting cells. Brucella spp., which is an intracellular facultative and stealthy pathogen, is able to evade the bactericidal activities of professional phagocytes. Several studies have demonstrated that Brucella can survive and replicate intracellularly, thereby provoking impaired maturation of DCs. Therefore, the interaction between DCs and Brucella becomes an interesting model to study the immune response. In this review, we first will describe the most common techniques for DCs differentiation in vitro as well as general features of brucellosis. Then, the interaction of DCs and Brucella, including pathogen recognition, molecular mechanisms of bacterial pathogenesis, and intracellular trafficking of Brucella to subvert innate response, will be reviewed. Finally, we will debate diversity in immunological DC response and the controversial role of DC activation against Brucella infection.

Neonatal bacteremia remains the major cause of infectious diseases-related death, especially in preterm newborns. Gram-positive bacteria are the main causative agent of neonatal bacteremia and exhibit a high risk of causing pneumonia and/or meningitis. The pathogenesis of bacteremia in preterm newborn is poorly understood. Current neonatal models of bacterial infection have been used to study the disease mechanisms; however, these studies employed mice of several days of age that could be less comparable to the bacteremia in preterm infants. In this study, we infected intravenously 0-day-old BALB/c mice with different inocula of Staphylococcus aureus, Streptococcus agalactiae or Enterococcus faecalis. We found that the mortality of the newborn mice was inoculum-dependent and also bacterial species-dependent. We observed bacterial burden in the lung, liver, brain, kidney and spleen of the infected animals. The lung was the tissue with the greatest bacterial burden and cellular infiltration in animals infected with the three bacteria evaluated. We found increased production of IL-6 and TNFα in the lung from newborn mice at 3 days post-infection. This neonatal model shows bacterial dissemination to the lung and will be useful for promote a better understanding of the pathophysiology of neonatal pneumonia.

Estrogens demonstrate biological activity in numerous organ systems, including the immune system, and exert their effects through estrogen receptors (ER) of two types: intracellular ERα and ERβ that activate transcriptional factors and membrane G protein-coupled ER GPER. The latter is capable to mediate fast activation of cytosolic signaling pathways, influencing transcriptional events in response to estrogens. Tamoxifen (TAM), widely used in chemotherapy of ERα-positive breast cancer, is considered as an ERα antagonist and GPER agonist. TAM was shown to possess “off-target” cytotoxicity, not related to ER in various tumor types. The present work was designed to study biological effects of TAM on the glucocorticoid (GC)-resistant cell line Jurkat, derived from acute lymphoblastic leukemia of T lineage (T-ALL). We have shown that T-ALL cell lines, in contrast to healthy T cells, express only GPER, but not ERα or ERβ. TAM compromised mitochondrial function and reduced the viability and proliferation of Jurkat cells. Additionally, TAM induced autophagy in a GPER-dependent manner. Gene expression profiling revealed the up-regulation of autophagy-related gene ATG5. Interestingly, TAM sensitized Jurkat cells to dexamethasone (DEX) treatment, which may be related to its capacity to cause autophagy. We suggest that TAM-based adjuvant therapy may represent a novel strategy in T-ALL patients handling.

Mast cells play an essential role in different immunological phenomena including allergy and infectious diseases. Several bacteria induce mast cell activation leading to degranulation and the production of several cytokines and chemokines. However, mast cells also have different microbicidal activities such as phagocytosis and the release of DNA with embedded granular proteins known as Mast Cell Extracellular Traps (MCETs). Although previous reports indicate that extracellular bacteria are able to induce MCETs little is known if intracellular bacteria can induce these structures. In this work, we evaluated MCETs induction by the intracellular bacteria Listeria monocytogenes. We found that mast cells released DNA after stimulation with L. monocytogenes, and this DNA was complexed to histone and tryptase. Before extracellular DNA release, L. monocytogenes induced modifications to the mast cell nuclear envelope and DNA was detected outside the nucleus. L. monocytogenes stimulated mast cells to produce significant amounts of reactive oxygen species (ROS) and blocking NADPH oxidase diminished DNA release by mast cells. Finally, MCETs showed antimicrobial activity against L. monocytogenes that was partially blocked when β-hexosaminidase activity was inhibited. These results show that L. monocytogenes induces mast cells to produce microbicidal MCETs, suggesting a role for mast cells in containing infection beyond the induction of inflammation.

Coronary endothelial dysfunction is associated with atherosclerosis and myocardial infarction in subjects with type 2 diabetes mellitus (T2DM). Vascular endothelial cells are referred to as small and polygonal mononuclear cells. However, multi-nucleated and large endothelial cells (named as multinucleated variant endothelial cells [MVECs]) have been reported in the aorta, wherein their abundance correlates with atherosclerosis severity. The role of MVECs in coronary endothelium remains obscure. We hypothesized that simulated diabetic conditions increase the number of MVECs and affect their mitochondrial structure/function in cultured coronary endothelium. The in vitro model of diabetes consisted in the treatment of bovine coronary artery endothelial cells (BCAECs) with high-insulin (100 nmol/L, HI) for three days followed by high-glucose (20 mmol/L, HG) and HI for nine additional days. Simulated diabetic conditions increased the abundance of MVECs compared to normal glucose (NG, 5.5 mM). MVECs had a higher nucleic acid content (7.2-Fold), cell diameter (2.2-Fold), and cell area (11.4-Fold) than mononuclear cells. Immunodetection of von-Willebrand factor (endothelial cell marker) in MVECs was positive. The mitochondrial mass was reduced, and mitochondrial membrane potential increased in mononuclear cells cultured in HG+HI compared to mononuclear cells grown in NG. However, the opposite mitochondrial findings were noted in MVECs compared to mononuclear cells. Mass spectrometry-based quantitative proteomic and gene ontology analysis suggested augmented mitochondrial autophagy, apoptosis, and inflammation suppression in cells cultured under HG+HI compared to NG conditions. These findings show that simulated diabetes increases the abundance of MVECs, and that mitochondrial structure and function are differentially affected between MVECs and mononuclear cells.

Background aims Cell therapy in neurological disability after traumatic brain injury (TBI) is in its initial clinical stage. We describe our preliminary clinical experience with three patients with diffuse axonal injury (DAI) who were treated with intrathecal administration of autologous mesenchymal stromal cells (MSCs). Methods Three patients with established neurological sequelae due to DAI received intrathecally autologous MSCs. The total number of MSCs administered was 60 × 10 6 (one patient), 100 × 10 6 (one patient) and 300 × 10 6 (one patient). Results All three patients showed improvement after cell therapy, and subsequent studies with 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) showed a diffuse and progressive increase in brain glucose metabolism. Conclusion Our present results suggest benefit of intrathecal administration of MSCs in patients with DAI, as well as a relationship between this type of treatment and increase in brain glucose metabolism. These preliminary findings raise the question of convenience of assessing the potential benefit of intrathecal administration of MSCs for brain diseases in which a decrease in glucose metabolism represents a crucial pathophysiological finding, such as Alzheimer's disease (AD) and other dementias.

We have reported on the capacity of (−)-epicatechin ((−)-EPI) to stimulate mitochondrial biogenesis (MiB) in mouse skeletal muscle (SkM). However, the mechanisms mediating the effects of (−)-EPI are not fully understood. We previously identified a role of the G-protein coupled estrogen receptor (GPER) in modulating the vascular effects of (−)-EPI. We therefore tested the hypothesis that GPER mediates (at least in part) the stimulatory effects of (−)-EPI on MiB in SkM cells. As an in vitro model, we employed mouse SkM-derived C2C12 myoblasts differentiated into myotubes. Using confocal microscopy, we detected GPER at the cell surface and cytoplasm in C2C12 myotubes. Treatment with (−)-EPI (3 and 10 µM) resulted in the stimulation of MiB as per increases in mitochondrial inner (MitoTracker Red FM fluorescence staining) and outer membrane (porin protein levels) markers, transcription factors involved in MiB stimulation (i.e., nuclear respiratory factor-2 [NRF-2] and mitochondrial transcription factor A [TFAM] protein levels) and citrate synthase (CS) activity levels. (−)-EPI-treated myotubes were longer and wider compared to vehicle-treated myotubes. The effects of (−)-EPI on myotube mitochondria and cell size were larger in magnitude to those observed with the GPER agonist G-1. The chemical blockade and down-regulation (siRNA) of GPER evidenced a partial and complete blockade of measured endpoints following (−)-EPI- or G-1-treatment, respectively. Altogether, results indicate that GPER is expressed in muscle cells and appears to mediate to a significant extent, the stimulatory effects of (−)-EPI on MiB. Thus, GPER activation may account for the stimulatory effects of (−)-EPI on SkM structure/function.

We evaluated the effects of a non-hepatotropic parasite infection (Taenia crassiceps) on the outcome of acetaminophen-induced acute liver failure in mice. Uninfected and T. crassiceps infected mice orally received either 300 mg/kg acetaminophen or water as vehicle (n = 5 per group). Survival analysis, hepatocyte necrosis, alanine aminotransferase (ALT) levels, CYP2E1 protein, interleukin (IL-) 5, and IL-6 were assessed for all groups. All infected mice died within 16 h after exposure to acetaminophen (Tc+APAP group), whereas only one-third of uninfected animals exposed to acetaminophen (APAP group) died. Uninfected (Control group) and infected (Tc group) mice that received the vehicle showed no liver damage. Tc+APAP mice exhibited massive liver necrosis characterised by marked balloning degeneration of hepatocytes and higher serum ALT compared to Control, Tc, and APAP animals. Liver tissue from Tc+APAP mice also displayed increased expression of CYP2E1 protein and higher mRNA and protein levels of IL-5 and IL-6 compared to the other groups. These findings suggest that non-hepatotropic parasite infections may increase mortality following acute liver failure by promoting hepatocyte necrosis via IL-5 and IL-6-dependent CYP2E1 overproduction. This study identifies new potential risk factors associated with severe acute liver failure in patients.

To ascertain the in vivo role of mycobacterial lipids phthiocerol dimycocerosates (PDIM) in experimental murine tuberculosis (Tb), airways infection was used to compare the parental virulent clinical isolate MT103 with its mutant fadD26, lacking PDIM. Lungs were assessed as the Tb-target organ and mediastinal lymph nodes as the corresponding lymphoid tissue, in order to quantify: the major T-cell subsets (CD4+/CD8+/gammadelta+) and their activation kinetics, bacillary burden, and in vivo cytotoxicity against inoculated target cells loaded with mycobacterial Ags. After 4 weeks, infection augmented total and activated CD4+ and CD8+ T cells in lungs and nodes mainly with MT103, while gammadelta+ T cells increased earlier in nodes. MT103 bacillary burden was bigger and appeared earlier than the mutant fadD26, especially in the lung than in mediastinal nodes. At day 14 of MT103 infection, there was no cytotoxicity in lungs and nodes; while with fadD26 there was some in the nodes. At day 21 of MT103 infection, important cytotoxicity was detected only in lungs; while with fadD26 both tissues showed important activity. Interestingly, unlike the infection with fadD26, cytotoxicity under MT103 fell considerably in the target organ (lung) from days 21 to 60, the advanced phase. Although upon airways infection both mycobacteria behaved similarly regarding T cell (CD4/CD8/gammadelta) stimulation kinetics; they differed in the magnitude of these responses, in the bacterial load within tissues, and to trigger in vivo cytotoxicity in lungs and regional lymph nodes. This highlights the relevance of certain mycobacterial lipids to modify crucial effector branches of immunity.

Dengue virus (DENV) has four serotypes, which can cause from asymptomatic disease to severe dengue. Heterologous secondary infections have been associated to a greater risk of potentially fatal dengue due to non-neutralizing memory antibodies (Abs), which facilitate the infection, such as anti-precursor membrane (prM) Abs, among other mechanisms. Usually, class-switched memory Abs are generated mainly through germinal centers (GCs). However, the cellular events underlying these Ab responses to DENV, especially during repeated/secondary infections, have been poorly studied. We wanted to know whether there is involvement of GC reactions during cutaneous DENV infection and whether there is any sort of preferential Ab responses to defined viral proteins. Intradermal DENV inoculation at a relatively low dose efficiently infects immune-competent BALB/c mice, inducing higher quantities of DENV-specific GC B cells and larger GCs than the control conditions. Interestingly, GCs exhibited as much prM as envelope (E) and non-structural 3 viral proteins in situ. Intriguingly, despite the much larger abundance of E protein than of prM protein in the virions, infected animals showed similar amounts of circulating Abs and Ag-specific GC B cells both for prM and for E proteins, even significantly higher for prM. To the best of our knowledge, there are no reports of the GC responses during DENV infection. This relatively stronger anti-prM response could be triggered by DENV to preferentially promote Abs against certain viral proteins, which might favor infections by facilitating DENV invasion of host cells. It is thus conceivably that DENV might have evolved to induce this kind of Ab responses.

Background Actinic Prurigo (AP) is a chronic pruritic dermatosis of unknown cause affecting sun exposed skin in defined ethnic groups with characteristic MHC alleles. However, the cutaneous dendritic cells have not been assessed. Objective To assess in situ the epidermal Langerhans Cell (LC) status in Actinic Prurigo. Study design Fresh skin samples from three AP patients were used to evaluate in situ the epidermal LC, comparing lesional and non-lesional sites in each subject. Setting AP patients attending the Dermatology Department at the Hospital M. Gea-Gonzalez in Mexico city. Methods Lesional and non-lesional skin samples were taken from each subject to prepare both epidermal sheets and conventional tissue sections. Three markers restricted to LC in epidermis (CD1a, ATPase, MHC-II) were used to quantify the LC per area in epidermal sheets. Results Compared to non-lesional skin from the same subject, a significant reduction in the number of LC per area of epidermis was found in lesional skin; with any of the three markers evaluated. Conclusion The frequency of epidermal LC decreases importantly in lesional skin from AP patients.

Convenios con empresa. En el proyecto se realiza el seguimiento de la construcción de un edificio que se compone de 3 sótanos para aparcamientos, planta baja sin uso definido y 4 plantas (incluyendo azotea) para 8 viviendas

A three-dimensional model of the alphaX I-domain of the horse integrin CD11c from dendritic cells provided information for selecting two segments of the primary structure for peptide synthesis. Peptide 1 contains 20 amino acids and peptide 2 has 17 amino acid residues. The first spans from position Thr229 to Arg248 of an alpha-helix segment of the structure, whereas peptide 2 goes from Asp158 to Phe174 and corresponds to an exposed segment of the loop considered to be the metal ion-dependent adhesion site. Murine polyclonal antisera against both peptides were generated and assayed in peripheral blood cell suspensions and in cryosections of horse lymph nodes. Only the serum against peptide 2 was capable of identifying cells in suspension and in situ by immunohistochemistry, some with evident dendritic morphology. Using this approach, an immunogenic epitope exposed in CD11c was identified in cells from horse lymph node in situ.

Neutrophils are one the earliest, crucial innate defenses against innumerable pathogens. Their main microbicidal activities include phagocytosis and degranulation, with many pharmacologically active molecules contributing to inflammation. Recently, a novel antimicrobial mechanism was discovered; the Neutrophil Extracelullar Traps (NETs) formed by extrusion of DNA and associated molecules (histones, elastase, antimicrobial peptides, among others) which trap and kill microorganisms. Since NETs were recently described, research has focused on their induction and microbicidal properties, and recently on disease involvement. However, the functional consequences of NETs interacting with other immune cells, either resident or recruited during early inflammation, have not been assessed. We therefore investigated the consequences of exposing two major APCs, macrophages (Mfs) and conventional Dendritic Cells (cDCs) to NETs. Our data revealed that at early times (30 min), both Antigen Presenting Cells (APCs) showed induction of important costimulatory molecules (CD80, CD86). Unexpectedly, however, at later times (6 and 24 hours) NETs apparently triggered a cell death process in these APCs by a caspase- and Apoptosis induced factor (AIF)-dependent pathway, suggesting mitochondrial damage. By rhodamine-123 labelling we found that in both APCs, relatively prolonged exposure to NETs or their components importantly decreased the mitochondrial membrane potential. Ultrastructural analysis confirmed mitochondrial alterations in both APCs. Our results would suggest that early in inflammation, NETs can activate the two main APCs (Mfs and cDCs), but as the process continues, NETs can then initiate apoptosis of these cells through mitochondrial harm. Conceivable, this “late” induction of cell death in these two APCs might start limiting an ongoing inflammatory process to control it. Electronic supplementary material The online version of this article (doi:10.1186/s40064-015-0932-8) contains supplementary material, which is available to authorized users.

El estudio comparativo del sistema inmunológico en especies distintas al Homo sapiens nos ha permitido descubrir nuevos mecanismos de la inmunidad y comprender los ya existentes, con la finalidad de generar conocimientos nuevos que, entre otras ventajas, podrían derivar en estrategias terapéuticas útiles en el área biomédica. Una de las formas de vida ancestrales para estudiar el sistema inmunológico es el tiburón, un organismo en el que se han identificado moléculas del sistema inmune adaptativo como el receptor de células B (BCR) y células T (TCR), el complejo mayor de histocompatibilidad (MHC) y el sistema activador de la recombinación (RAG), además de poseer un tipo de inmunoglobulinas (IgNAR) con propiedades únicas como alta solubilidad y estabilidad biofísica. Con la finalidad de entender mejor la inmunología de este organismo, el presente trabajo aborda aspectos del fenotipo y función en células del sistema inmune innato del tiburón Heterodontus francisci, una especie con un origen evolutivo de aproximadamente 250 millones de años. Después de la extracción de sangre y el aislamiento de leucocitos, se determinó mediante citometría de flujo que existen anticuerpos monoclonales para proteínas de mamífero que generan una reacción cruzada contra antígenos de tiburón, observando una relación estímulo-fenotipo dada por un aumento en la detección de proteínas asociadas con linfocitos B (CD19), fagocitos especializados (CD206) y una proteína asociada con linfocitos T (CD5) posterior a la exposición con tres especies de bacterias (Escherichia coli, Staphylococcus aureus y Vibrio harveyi). Respecto a los ensayos de la capacidad de engullimiento de leucocitos de tiburón evaluados nuevamente por citometría de flujo, se evidenciaron diferencias en relación con el tamaño y granularidad de las regiones leucocitarias y el estímulo adicionado, observamos que E. coli es un fuerte inductor de los procesos de internalización. Finalmente, utilizando microscopía de epifluorescencia, se observó en los leucocitos la inducción de estructuras semejantes a trampas extracelulares dependientes del estímulo con S. aureus; hipotetizamos que este efecto está mediado, como en los mamíferos, por algún tipo de TLR, fenómeno que sugiere que puede ser un mecanismo de defensa sumamente antiguo y conservado. La respuesta celular en leucocitos de H. francisci incluye la expresión de proteínas de membrana que brindan identidad a los leucocitos y la activación de funciones innatas... Comparative studies between humans (Homo sapiens) and other species have led to the discovery and understanding of new and existing mechanisms of the immune system. These discoveries help unveil and solve current issues, and allow the generation of knowledge that could lead to new therapeutic strategies in the biomedical field. Sharks are one of the most ancient vertebrate subclasses in which to study the immune system, an organism with adaptive immune system molecules like B (BCR) and T (TCR) cells receptor, major histocompatibility complex (MHC) and the recombination-activating gene (RAG), also they have a special type of immunoglobulins (IgNAR) with unique properties including high solubility and biophysical stability. In order to have a better understanding of shark immunology, this work aims to study the functional and phenotypic aspects of innate immune system cells of the Heterodontus francisci shark, a species with approximately 250 million years of evolutionary divergence. In the present study, we detected a possible cross reactivity between monoclonal antibodies against mammal proteins and shark antigens using flow cytometry. We observed a phenotype-stimuli relationship characterized by an increase of proteins associated to B lymphocyte (CD19), professional phagocyte (CD206) and T-B lymphocyte (CD5) populations after bacterial stimulation (Escherichia coli, Staphylococcus aureus y Vibrio harveyi). Regarding leukocyte engulfment capacity assessed by flow cytometry, it was shown that there are many differences between size and granularity between leukocyte regions and the added stimuli; it was observed that E. coli is a strong inductor of internalization processes. Finally, we observed Extracellular Trap-like (ETs) structures in shark leukocytes by epifluorescence microscopy. These ETs were dependent on S. aureus stimuli, and we infer that this mechanism is mediated by some type of TLR, similar to mammals. This suggests that ETs may be a very ancient and conserved mechanism. The cellular response in H. francisci leukocytes includes membrane protein expression that provides identity to leukocytes and specific innate function activation; this response is dependent and varies according to the bacterial stimuli to which cells are exposed. In many cases, the immune response keeps similarities with stimulus-response processes observed in mammals, suggesting that there are evolutionarily conserved immune elements and mechanisms between two very distant sp